The most recent information on VCAM1 is here. Click here for the function of VCAM1. Edit this page in Wiki Genes - VCAM1 or see Wiki Gene. In contrast, VCAM-1 expression was 15% of that induced by TNF. Paper-839742. ICAM-1 and VCAM-1 mRNA expression were also inhibited by KGF. Paper-9701163. VCAM-1 engagement also stimulated a rapid increase in PI3K activity. Paper-8688204. In normal controls, PECAM was intensely expressed and VCAM-1 was weakly expressed. Paper-688887. VCAM-1 was suppressed to the greatest extent followed by E-selectin and then ICAM-1. Paper-15521416. Crosslinking of CD44 on human osteoblastic cells upregulates ICAM-1 and VCAM-1. Paper-9860348. PrMC adhesion to IL-4- activated HUVECs was totally alpha4-integrin- and VCAM-1-dependent. Paper-9201920. Notably, Hcy increased VCAM-1 protein expression induced by CD40L in HUVECs (p = 0.0046). Paper-13271664. MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1. Paper-12727801. APE1/ref-1 overexpression also suppressed expression of VCAM-1 induced by TNF-alpha. Paper-11353586. This correlated with a 75% reduction in TNF-alpha- induced VCAM-1 expression. Paper-1258710. AM inhibited the VEGF- induced protein and mRNA expression of ICAM-1, VCAM-1, and E-selectin. Paper-9932996. Combination of TNF-alpha and IFN-gamma synergized to induce high levels of VCAM-1 expression. Paper-7585573. VCAM-1 was expressed in 24 out of 88 tumors (27.3%) and NCAM only in 14 out of 87 tumors (16%). Paper-2110883. IL-13 regulates vascular cell adhesion molecule-1 expression in human osteoblasts. Paper-10018473. CD81 also colocalized with ICAM-1 and VCAM-1 in the adhesion rings around bound monocytes. Paper-13495630. Such effects were accompanied by a boosting of insulin effect on VCAM-1 surface expression. Paper-13602773. Insulin potentiates cytokine- induced VCAM-1 expression in human endothelial cells. Paper-12912812. In contrast, exogenous uPA stimulated ICAM and VCAM adhesion of airway eosinophils. Paper-12230643. Inhibition of TNF-alpha induced ICAM-1, VCAM-1 and E-selectin expression by selenium. Paper-9399374. TNF-alpha could significantly induce CCL2, ICAM-1 and VCAM-1 expression of PTEC. Paper-12944881. For eosinophils from allergic subjects, IL-5 also inhibited Mn(2+)- induced adhesion to VCAM-1. Paper-454262. TNF and IL-1 were equivalent in their ability to induce VCAM mRNA and protein expression by HUVECs. Paper-536464. Arsenite enhances tumor necrosis factor-alpha- induced expression of vascular cell adhesion molecule-1. Paper-11156986. Notably, TRPC3 knock-down resulted in a dramatic reduction of ATP- induced VCAM-1 and monocyte adhesion. Paper-13051784. C5b-9-induced VCAM-1 expression may thus involve an NO/ cGMP- regulated NF-kappaB translocation mechanism. Paper-8339253. OSM enhanced cell surface expression of ICAM-1, but not VCAM-1, on endothelial cells and RASFs. Paper-12288663. Involvement of MAPKs and NF-kappaB in LPS- induced VCAM-1 expression in human tracheal smooth muscle cells. Paper-13193892. Caveolin-1 is associated with VCAM-1 dependent adhesion of gastric cancer cells to endothelial cells. Paper-12045459. ICAM-1 expression was up-regulated and VCAM-1 induced in muscle capillaries of dermatomyositis samples. Paper-971774. ICAM-1 and VCAM-1 expression induced by TNF-alpha are inhibited by a glutathione peroxidase mimic. Paper-1595975. TNF-alpha- induced VCAM, ICAM, and MCP-1 expression (4h) preceded PAPP-A expression (24h). Paper-14307978. TGF-beta and endothelial cells inhibit VCAM-1 expression on human vascular smooth muscle cells. Paper-280956. Finally, PTEN significantly prevented monocyte adhesion to TNF-α- induced ECs probably through VCAM-1 regulation. Paper-15440646. In addition, LPS-induced VCAM-1 expression was significantly blocked by a specific NF-kappaB inhibitor helenalin. Paper-13193892. Transforming growth factor beta ( TGFbeta) had no effect on ICAM-1 and decreased the expression of VCAM-1. Paper-1482961. NF-kappaB inhibitor, PDTC dose dependently inhibited the TNF-alpha induced VCAM-1 mRNA expression. Paper-9327556. Mite antigens enhance ICAM-1 and induce VCAM-1 expression on human umbilical vein endothelium. Paper-10067255. Both PPARalpha activators decreased cytokine- induced VCAM-1 mRNA expression without altering its mRNA half-life. Paper-1892647. DHT increased VCAM-1 promoter activity via NF-kappaB activation without affecting VCAM-1 mRNA stability. Paper-10384941. RORalpha1 and RORalpha4 suppress TNF-alpha- induced VCAM-1 and ICAM-1 expression in human endothelial cells. Paper-10373893. Cilostazol strongly inhibited tumor necrosis factor (TNF)-alpha- induced expression of VCAM-1 protein and its mRNA. Paper-9043292. Furthermore, TNF-alpha- induced VCAM-1 expression was significantly blocked by a selective NF-kappaB inhibitor helenalin. Paper-11388102. NCAM and ICAM were constitutively expressed on HCECs whereas VCAM-1, ELAM-1, and CD44 were absent from normal HCECs. Paper-7302879. Thus, AM inhibits VEGF- stimulated ICAM-1 and VCAM-1 expression through a phosphatidylinositol 3'-kinase/Akt pathway. Paper-9932996. The leukocyte integrin alpha D beta 2 binds VCAM-1: evidence for a binding interface between I domain and VCAM-1. Paper-1964540. IL-4- induced oxidative stress upregulates VCAM-1 gene expression in human endothelial cells. Paper-8691034. P2Y2 antisense oligonucleotides inhibited VCAM-1 expression induced by UTP but not by tumor necrosis factor-alpha. Paper-9779916. ILK knockdown impaired LPS- mediated endothelial activation by preventing the induction of ICAM-1 and VCAM-1. Paper-15249024. Our experiments show that IFN amplifies TNF- induced VCAM-1 expression at the transcriptional level by an IRF-1-dependent pathway. Paper-1465781. Specific inhibitors for JNK and NF-kappaB also inhibited TNF-alpha- induced ICAM-1 and VCAM-1 expressions in HUVEC. Paper-10209480. Specific pharmacological inhibitors of JNK and p38 but not ERK significantly inhibited TNF- induced VCAM expression. Paper-10010175. In fact, these LPL effects on VCAM1 were absent in endothelial cells isolated from PPAR alpha-deficient mice. Paper-9879223. In this context, the observed suppression of the TNF-alpha induced VCAM-1 expression is likely to play an essential role. Paper-10262388. Talin 1 and paxillin facilitate distinct steps in rapid VLA-4- mediated adhesion strengthening to vascular cell adhesion molecule 1. Paper-13406965. PPARalpha activators inhibit cytokine- induced vascular cell adhesion molecule-1 expression in human endothelial cells. Paper-1892647. IL-4 synergized with LPS to induce VCAM-1 expression at 24, 48, or 72 h, whereas IL-4 alone induced expression at 72 h only. Paper-1429165. TNF-alpha- induced increased expression of ICAM-1, E-selectin, and VCAM-1 mRNA was significantly depressed by 15-HPETE. Paper-873501. Removal of cell-bound uPA and/or addition of exogenous uPA had no effect on blood eosinophil adhesion to ICAM-1 or VCAM-1. Paper-12230643. However, the role of AP-1 in LPS- induced VCAM-1 expression in human tracheal smooth muscle cells (HTSMCs) is not known. Paper-13837505. GPx-1 deficiency also transiently augmented LPS- induced vascular cell adhesion molecule-1 ( VCAM-1) expression. Paper-15171898. The stability of TNF-alpha- induced ICAM-1 and VCAM-1 expression at mRNA and protein level was not altered by cicaprost. Paper-1274439. We show that IFN-alpha and -gamma enhance TNF- induced VCAM-1 mRNA transcription and protein expression in human endothelial cells. Paper-1465781. IL-18 significantly enhanced ICAM-1 and VCAM-1 expression on endothelial cells and RA synovial fibroblasts. Paper-8960423. Human IL-8 regulates smooth muscle cell VCAM-1 expression in response to endothelial cells exposed to atheroprone flow. Paper-13718418. CONCLUSIONS: ET-1 can stimulate HMC to produce TNF alpha, ICAM-1 and VCAM-1, and thereby induce inflammatory effects. Paper-1426068. Genetic analysis reveals the existence of activator protein-1 ( AP-1) binding site on VCAM-1 promoter region. Paper-13837505. These findings correlated with an enhancement of MT1-MMP fibrinolytic activity in monocytes bound to FN, VCAM-1, or ICAM-1. Paper-10775134. Insulin receptor small interfering RNA knockdown abolished insulin- stimulated increases of ICAM-1 but not VCAM-1. Paper-13785631. Steady state mRNA levels of TNF-alpha- induced VCAM-1 and E-selectin are significantly reduced by physiological concentrations of HDLs. Paper-411759. Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB in IL-1beta- induced VCAM-1 expression in human tracheal smooth muscle cells. Paper-11101696. Mechanisms of VCAM-1 and fibronectin binding to integrin alpha 4 beta 1: implications for integrin function and rational drug design. Paper-389294. Reverse transcription-polymerase chain reaction showed that VCAM-1 mRNA was induced in IL-4-treated HUVEC in a time- and dose-dependent manner. Paper-8691034. CONCLUSION: Our results indicate that upregulation of PTEN by CKD712 selectively inhibit VCAM-1 expression in LPS-treated HUVECs. Paper-14123281. Histologically unaffected areas of MS brain expressed less VCAM-1, ICAM-1, and E-selectin than did microvessels from periplaque zones. Paper-8197809. In transient transfection studies, cilostazol inhibited TNF-alpha- induced transcriptional activation of VCAM-1 promoter. Paper-9043292. Nuclear factor-kappaB ( NF-kappaB) is known to regulate the expression of adhesive and chemotactic molecules including VCAM-1 and IL-8. Paper-10295016. Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4- induced VCAM-1 expression. Paper-8691034. IL-1beta-induced VCAM-1 expression was significantly blocked by the specific NF-kappaB inhibitors helenalin and pyrrolidine dithiocarbamate. Paper-11101696. C-reactive protein induces VCAM-1 gene expression through NF-kappaB activation in vascular endothelial cells. Paper-11398387. The P2Y2 nucleotide receptor mediates vascular cell adhesion molecule-1 expression through interaction with VEGF receptor-2 ( KDR/Flk-1). Paper-10534020. TNF-alpha- stimulated human VSMCs demonstrate increased binding of T lymphocytes that is totally VCAM-1 mediated. Paper-280956. In vitro exposure to IL-13 of human umbilical vein EC induced surface expression of vascular cell adhesion molecule-1 ( VCAM-1). Paper-8225670. Eosinophil tethering to interleukin-4- activated endothelial cells requires both P-selectin and vascular cell adhesion molecule-1. Paper-1654825. The authors observed a marked increase in ICAM-1 and VCAM-1 expression on HUVEC stimulated for 24 h by TNF-alpha (10 ng/ml) or IL-1 (20 ng/ml). Paper-974867. Further analysis demonstrated that HDAC3 plays a significant role in the regulation of TNF-alpha- mediated VCAM-1 expression. Paper-12320244. Cilostazol represses vascular cell adhesion molecule-1 gene transcription via inhibiting NF-kappaB binding to its recognition sequence. Paper-9043292. Further, chromatin immunoprecipitation (ChIP) assay showed that PTEN targets GATA-6 but not IRF-1 binding to VCAM-1 promoter. Paper-15440646. The GPx mimic BXT-51072 strongly inhibits the TNFalpha- induced and cycloheximide-sensitive expression of ICAM-1 and VCAM-1. Paper-1595975. Histamine augmented TNF-alpha- and thrombin- induced vascular cell adhesion molecule 1 ( VCAM-1) expression to a similar extent. Paper-12285969. These results suggest that in HTSMCs, activation of MAPK pathways, NF-kappaB, and p300 is essential for TNF-alpha- induced VCAM-1 expression. Paper-11388102. The mechanism of suppression may involve inhibition of NF-kappaB- mediated up-regulation of VCAM-1 expression induced by atherogenic stimuli. Paper-10303440. Only a fraction of microvascular loops were positive for ICAM-1, ELAM-1 or VCAM-1 when compared to the constitutively expressed PECAM-1. Paper-8212908. Transfection with dominant negative mutants of MEK1/2, ERK1, ERK2, p38, and JNK attenuated TNF-alpha- induced VCAM-1 expression. Paper-11388102. Both the mb and the s forms of VCAM-1 and ICAM-1 were upregulated by TNF-alpha; however, the stimulation of the s forms was delayed in time. Paper-1760815. Pharmacologic inhibition of Rho kinase signaling blocked LPA-induced p65 phosphorylation and suppressed ICAM-1 and VCAM-1 expression. Paper-15247565. Furthermore, we found that RORalpha1Delta attenuated the inhibitory actions of 15d-PGJ2 on TNF-alpha- induced VCAM-1 and ICAM-1 expression. Paper-11066143. Further investigation revealed that ICAM-1 and VCAM-1 mRNA and protein are induced by TNFR1 (but not TNFR2) in a wholly NF-kappaB-dependent manner. Paper-13193888. Hyperosmotic stimuli inhibit VCAM-1 expression in cultured endothelial cells via effects on interferon regulatory factor-1 expression and activity. Paper-9509686. Soluble vascular cell adhesion molecule-1 is independently associated with soluble tumor necrosis factor receptor 2 in Japanese type 2 diabetic patients. Paper-13106907. These results indicate that VCAM-1 and ICAM-1 expression can be differentially regulated and suggest tissue specific regulation of VCAM-1 expression. Paper-7212475. Studies with actinomycin D indicate that FP treatment accelerated the degradation of TNF-alpha- induced VCAM-1 mRNA. Paper-1824393. Phosphatidylinositol 3-kinase ( PI3K) and nuclear factor-kappaB ( NF-kappaB) inhibitor inhibit both ICAM-1 and VCAM-1 expression induced by TWEAK. Paper-12313660. VCAM-1 induction was partially suppressed by p44/42 MAPK (PD-098059) but unaffected by c-Jun NH2-terminal kinase (SP-600125) inhibition. Paper-13785064. The P2Y2 nucleotide receptor mediates UTP- induced vascular cell adhesion molecule-1 expression in coronary artery endothelial cells. Paper-9779916. CONCLUSION: The results of our study suggest that genetic variation in ER gene may influence blood levels of VCAM-1 in women after the menopause. Paper-12628055. The parenchymal adhesion molecule VCAM-1 was found to be downregulated in kidneys of MRL-Fas(lpr) IL-6 -/- compared to IL-6-intact mice. Paper-14196086. Stable ( HEK293 cells) or transient (HCAECs) overexpression of TRPC3 enhanced TNFalpha- induced VCAM-1 compared to wild-type cells. Paper-15106588. Moreover, CRP increased VCAM-1 promoter activity, indicating that CRP induces VCAM-1 mRNA expression at the transcriptional level. Paper-11398387. Furthermore, P2Y2R activation mediated the up-regulation of VCAM-1 expression in HSG cells leading to increased adherence of lymphocytic cells. Paper-12488473. Membrane expression of adhesion molecules was also strikingly increased, with 80% of the cells expressing VCAM-1 and 65% expressing ELAM-1 upon incubation. Paper-8496541. In contrast, TNF was significantly more potent than IL-1 in inducing VCAM mRNA and protein expression by nasal mucosal microvascular endothelial cells. Paper-536464. Paradoxically, NAC exerted a positive effect on low shear-induced VCAM-1 expression and EC-Mn adhesion and only slightly downregulated NF-kappaB activation. Paper-1852745. These results demonstrate that MM cell adhesion to VCAM-1 upregulates MIP-1 production by MM cells to cause enhancement of osteoclastogenesis. Paper-13556604. Hypoxia up-regulated angiogenin and down-regulated vascular cell adhesion molecule-1 expression and secretion in human placental trophoblasts. Paper-11008912. In contrast, thrombin-mediated transactivation of a minimal promoter containing tandem VCAM-1 GATA motifs was inhibited by DN- PKC-zeta but not DN-PKC-delta. Paper-9844475. An in-house preparation of pure, active, and uncontaminated CyPA failed to induce endothelial TF or VCAM-1 expression; moreover, it was not chemotactic for HAEC. Paper-14386268. Angiopoietin-1 reduces VEGF- stimulated leukocyte adhesion to endothelial cells by reducing ICAM-1, VCAM-1, and E-selectin expression. Paper-9064399. No changes in VCAM-1 expression were induced by TNF-alpha, IL-4 or bFGF, whereas both TNF-alpha and IL-4 increased eotaxin release (p < 0.05). Paper-9472404. VCAM-1 interacted directly with moesin and ezrin in vitro, and all of these molecules colocalized at the apical surface of endothelium. Paper-9165193. Cicaprost as well as forskolin significantly inhibited TNF-alpha- and IL-1 beta- induced cell surface expression of ICAM-1 and VCAM-1. Paper-1274439. Specific antibodies to human VCAM and MAdCAM were used to confirm expression in control and MS nervous system specimens by immunohistochemistry. Paper-14218856. In addition, expression of superoxide dismutase by adenovirus suppressed TNF-alpha- induced VCAM-1, E-selectin, and ICAM-1 mRNA accumulation. Paper-9676674. Role of tyrosine kinase enzymes in TNF-alpha and IL-1 induced expression of ICAM-1 and VCAM-1 on human umbilical vein endothelial cells. Paper-974867. The IkappaB degradation, NF-kappaB nuclear translocation and VCAM-1 up-regulation induced by CRP were all inhibited by treatment with siRNA against CD32. Paper-11308432. Interleukin-4 and lipopolysaccharide synergize to induce vascular cell adhesion molecule-1 expression in human lung microvascular endothelial cells. Paper-1429165. RNA interference targeting VEGFR-2 or inhibition of VEGFR-2 tyrosine kinase activity abolishes P2Y(2)R- mediated VCAM-1 expression. Paper-10534020. In co-transfection assays, thrombin stimulation of a minimal promoter containing multimerized VCAM-1 NF-kappaB sites was inhibited by DN-PKC-delta but not DN- PKC-zeta. Paper-9844475. RESULTS: Puerarin inhibited the expression of TNF-alpha- induced ICAM-1, VCAM-1 and E-selectin proteins and mRNAs in HUVECs. Paper-14215437. The results show that LFA-1 andVLA-4 were expressed in HPPEPCs and ICAM-1 and VCAM-1 were expressed in vessel endothelium in ischemic tissues. Paper-12341437. These results indicated that differential regulation of AP-1 through PKCs-dependent MAPKs activation plays central roles in LPS- induced VCAM-1 expression. Paper-13837505. These results suggest that the presence of a co-stimulus such as LPS may be necessary for IL-4 to effectively induce VCAM-1 expression in lung microvasculature. Paper-1429165. The inhibition of SB at 10 microM on TNF-alpha- induced ICAM-1, VCAM-1 and E-selectin is likely due to the nonspecific effect of SB. Paper-13008844. Interestingly, the dominant-negative isoform of Rac1 was not selective but inhibited the TNF-alpha stimulation of the mRNA expression of VCAM-1 and ICAM-1. Paper-9457948. Transfection of endothelial cells with an oligonucleotide that decreases miR-126 permits an increase in TNF-alpha- stimulated VCAM-1 expression. Paper-12727801. VCAM-1 expression has been shown to be driven primarily by binding of nuclear factor-kappaB ( NF-kappaB) to two consensus binding sites in the promoter region. Paper-8793644. An upstream VCAM-1 gene regulatory region distinct from the NF-kappa B sites appears to function as an IL-1 alpha-mediated transcriptional repressor within HDMEC. Paper-462690. We report the definition of a functional regulatory element in the VCAM1 promoter interacting with the transcriptional activator interferon regulatory factor 1 ( IRF-1). Paper-218072. The anti-oxidant, N-acetyl cysteine, inhibited TNF-alpha- induced PAPP-A expression without altering the induction in VCAM, ICAM, and MCP-1. Paper-14307978. The present findings suggest that the benefits of statins in vascular disease may include the inhibition of expression of VCAM-1 and ICAM-1 through effects on NF-kappaB. Paper-10313650. The expression of ICAM-1 and VCAM-1 but not ELAM-1 mRNA was significantly induced with IL-1 beta in a concentration (1 fM - 1 nM)- and time (0.5 - 24 h)-dependent manner. Paper-340687. Binding of monocytes to TNF-alpha- activated human endothelial cells as well as to VCAM-1 or ICAM-1 also resulted in an increase of MT1-MMP expression. Paper-10775134. PTEN differentially regulates expressions of ICAM-1 and VCAM-1 through PI3K/Akt/GSK-3β/ GATA-6 signaling pathways in TNF-α-activated human endothelial cells. Paper-15440646. We could show that deletion of p38alpha gene did not affect TNF-alpha- induced ICAM-1 and VCAM-1 expression when compared with wild-type cells. Paper-13008844. It is concluded that PTEN selectively inhibits expression of VCAM-1 but not ICAM-1 through modulation of PI3K/Akt/GSK-3β/ GATA-6 signaling cascade in TNF-α-treated ECs. Paper-15440646. CONCLUSION(S): Changes in E(2) levels seen during gonadotropin stimulation significantly alter VCAM-1 expression and induce changes in serum IL-6 and TNF-alpha levels. Paper-13542574. Inhibitors of EGFR phosphorylation and metalloprotease activity abolished P2Y2R- mediated VCAM-1 expression and decreased lymphocyte binding to HSG cells. Paper-12488473. OBJECTIVE: The present studies addressed this important question and gathered mechanistic insight on the signaling coupling constitutive TRPC3 function to VCAM-1 expression. Paper-15106588. TNF-alpha and interleukin-1beta (IL-1beta) stimulated cell surface ICAM-1 expression, but not VCAM-1 expression, in human aortic smooth muscle cells (HASMCs). Paper-1936555. TNF/fMLP stimulation also produced a similar increase in CD49d- mediated adhesion of neutrophils to a vascular cell adhesion molecule-1 (VCAM-1)-coated surface. Paper-10253331. Together, these results suggest that in HTSMC, activation of p42/p44 MAPK, p38, JNK, and NF-kappaB pathways is essential for IL-1beta- induced VCAM-1 gene expression. Paper-11101696. Co-transfection and microinjection studies demonstrate that Oct-1 blocks tumor necrosis factor alpha- stimulated E-selectin and VCAM-1 expression. Paper-13144125. VCAM-1 was co-localized with Caveolin-1 and siRNA- mediated knockdown of Caveolin-1 expression significantly blocked the VCAM-1-dependent cell adhesion. Paper-12045459. VCAM-1 induced spontaneous EOS adhesion whereas EOS adhesion to ICAM-1 required a second signal, such as granulocyte macrophage colony-stimulating factor ( GM-CSF). Paper-1485210. Physiological concentrations of adiponectin dose-dependently inhibited TNF-alpha- induced THP-1 adhesion and expression of VCAM-1, E-selectin, and ICAM-1 on HAECs. Paper-2057157. CD11c/ CD18 expression is upregulated on blood monocytes during hypertriglyceridemia and enhances adhesion to vascular cell adhesion molecule-1. Paper-15583579. Integrin alpha 4 beta 1 can mediate both cell-cell and cell-extracellular matrix adhesion by binding to either fibronectin or vascular cell adhesion molecule 1 ( VCAM-1). Paper-389294. X-linked hydrocephalus and associated phenotypes are due to mutations in the L1CAM gene, which has been identified as a coding neural cell adhesion molecule. Paper-11220030. As a functional consequence, adhesion of U937 monocytes to TNF- stimulated HUVECs was markedly reduced by aspirin due to suppression of VCAM-1 and E-selectin upregulation. Paper-183363. Similarly, cross-linked MAbVLA-4 or VCAM-1 augmented Ca(2+)- mediated IL-8 secretion from THP-1 monocytes and was completely abolished by exposure to CsCl, an I(ir) blocker. Paper-9219320. IFN enhancement of TNF- induced expression is also seen using chloramphenicol acetyl transferase reporter genes linked to the minimal cytokine inducible VCAM-1 promoter. Paper-1465781. VCAM-1 is constitutively expressed by human MSC and its expression can be upregulated by interleukin-4 ( IL-4) and recombinant human tissue necrosis factor-alpha (rTNF-alpha). Paper-83811. We further demonstrated that inhibition of NF-kappaB completely blocked TNF-alpha- induced expression of ICAM-1, VCAM-1 and E-selectin. Paper-13008844. RT-PCR and promoter analysis revealed that HGF downregulated VEGF- mediated expression of ICAM-1 and VCAM-1 at the transcriptional level. Paper-10791313. This IL-1 beta- mediated induction of ICAM-1 and VCAM-1 expression was significantly inhibited in the presence of a NO donor 3-morpholino-sydnonimine (SIN-1) in a dose-dependent manner. Paper-1046992. There was some suggestion that the VCAM-1/VLA-4 adhesion pathway was expressed at higher levels in chronic MS lesions, while ICAM-1/LEA-1 was used more uniformly in lesions of all ages. Paper-199289. PTEN strongly inhibited VCAM-1 but not ICAM-1, however this inhibitory effect was reversed by co-transfection with constitutively active-Akt (CA-Akt-HA) in TNF-α-stimulated ECs. Paper-15440646. FP (10(-7) M) also inhibited VCAM-1 mRNA expression induced by TNF-alpha in primary human bronchial epithelial cells as assessed by reverse transcription-polymerase chain reaction. Paper-1824393. Signal transduction pathways involved in rheumatoid arthritis synovial fibroblast interleukin-18- induced vascular cell adhesion molecule-1 expression. Paper-9170419. Similar silencing or neutralizing of vascular cell adhesion molecule-1 alone did not have an effect but was shown to contribute to intercellular adhesion molecule-1 when tested simultaneously. Paper-12465813. OBJECTIVE: Our purpose was to determine expression of VCAM-1 in normal and inflamed skin and the effect on this of the T-cell-derived cytokine interferon gamma ( IFN-gamma). Paper-7881275. TNF-alpha enhanced ICAM-1 expression by synovial cells and endothelial cells, whereas VCAM-1 or E-selectin expression was not enhanced on either cell type. Paper-749670. Increased serum concentrations of VCAM-1 were associated with locally advanced and metastatic disease whereas ICAM-1 was significantly elevated both in local and in advanced/metastatic disease. Paper-1260155. A novel thiazolidinedione MCC-555 down-regulates tumor necrosis factor-alpha- induced expression of vascular cell adhesion molecule-1 in vascular endothelial cells. Paper-11508609. In summary, we demonstrate that arsenite enhances the TNF-alpha- induced VCAM-1 expression in HUVECs via regulation of AP-1 and NF-kappaB activities in a GSH-sensitive manner. Paper-11156986. Binding to ELAM-1 was inhibited by MoAb to ELAM-1 and binding to VCAM-1 was inhibited by MoAb to VCAM-1 or the alpha-chain of very late activation antigen-4 (VLA-4) ( CD49d). Paper-6927543. The role of SP-1 in IL-4- induced VCAM-1 expression was confirmed in HUVEC transfected with a reporter construct of the VCAM-1 promoter with mutated SP-1 binding site. Paper-8691034. MKP-1 induction was shown to be necessary for the antiinflammatory effects of shear stress because gene silencing of MKP-1 restored VCAM-1 expression in sheared ECs. Paper-12953174. The IL-1 beta- induced adhesion of SMCs for monocytes was partially inhibited by monoclonal anti-human ICAM-1 and anti-human VCAM-1 antibody, but not by anti-human ELAM-1 antibody. Paper-340687. Rapid expression of mRNA encoding vascular cell adhesion molecule-1 ( VCAM-1) was induced by tumor necrosis factor ( TNF) in fibroblast-like cells obtained from synovial tissue. Paper-7212475. TNF-alpha- induced the expression of vascular cell adhesion molecule-1 ( VCAM-1) and endothelial cell-selectin ( E-selectin) expression was inhibited in HUVEC pretreated with EGJ. Paper-15161313. Further functional studies confirmed that NOR1 mediates monocyte adhesion by inducing VCAM-1 and intercellular adhesion molecule-1 expression in endothelial cells. Paper-15372586. Conversely, IGF-I receptor blockade with either a neutralizing antibody or specific small interfering RNA eliminated insulin- induced VCAM-1 but not ICAM-1 production. Paper-13785631. Fluorescein isothiocyanate (FITC)-labeled anti- ICAM-1 and FITC- labeled anti- VCAM-1 were used to analyze the IL-1alpha- induced expression of ICAM-1 and VCAM-1 by flow cytometry. Paper-11364783. LPS, TNF-alpha, or IL-1 beta increased the overall intensity of surface staining and the percentage of cells expressing VCAM-1 in a time- and concentration-dependent manner. Paper-319558. Electrophoretic mobility-shift assay demonstrated that MCC-555 reduced the amount of nuclear factor-kappaB ( NF-kappaB) bound to its recognition site on the VCAM-1 promoter. Paper-11508609. At a functional level, preincubation of HGF resulted in inhibition of VEGF- induced vascular cell adhesion molecule (VCAM)-1-mediated monocyte adhesion to endothelial cells. Paper-13051786. METHODS AND RESULTS: In HCAECs, maneuvers that prevent Ca(2+) influx or knockdown of TRPC3 markedly reduced tumor necrosis factor (TNF)alpha- induced VCAM-1 and monocyte adhesion. Paper-15106588. Vascular cell adhesion molecule-1 expression in human intestinal microvascular endothelial cells is regulated by PI 3-kinase/Akt/ MAPK/ NF-kappaB: inhibitory role of curcumin. Paper-13785064. The cellular processes mediated by the interaction of alpha 4 beta 1 with Fn or VCAM-1 were inhibited by the CS1 peptide derived from the major alpha 4 beta 1 binding site on Fn. Paper-246990. It was found that part of the EC binding by these CD11a/ CD18-deficient clones was mediated by an interaction of very late Ag-4 (VLA-4) with vascular cell adhesion molecule-1 ( VCAM-1) on the EC. Paper-6927996. G-CSF- stimulated peripheral blood progenitor cells (PBPC) mobilization results in increased levels of circulating endothelial adhesion molecules that were most evident for VCAM-1 molecules. Paper-9608576. Selective inhibition of tumor necrosis factor- induced vascular cell adhesion molecule-1 gene expression by a novel flavonoid. Lack of effect on transcription factor NF-kappa B. Paper-831441. Furthermore, VCAM-1 mRNA induction was inhibited in TNF-alpha-stimulated SMCs, but not in differentiating SMCs, by pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB protein activation. Paper-1719910. PBMC and PBMC supernatants were highly potent at upregulating intercellular adhesion molecule-1 ( ICAM-1) and inducing expression of vascular cell adhesion molecule-1 ( VCAM-1) and E-selectin. Paper-1571080. The cytokine enhanced intercellular adhesion molecule-1 ( ICAM-1) expression and induced the expression of vascular cell adhesion molecule-1 ( VCAM-1) and E-selectin on endothelial cells. Paper-605948. Stimulation of PAPP-A expression by TNF-alpha was associated with significantly increased VCAM, ICAM, and MCP-1 expression but without major changes in other IGF system components. Paper-14307978. Conversely, in CB progenitors, anti- IL-15 mAb inhibited VCAM-1 and beta1 integrin expression without affecting gammac chain expression and, most important, up-regulated SDF-1 expression. Paper-9781046. METHODS AND RESULTS: Commercially available recombinant CyPA- induced expression of tissue factor (TF) and vascular cell adhesion molecule-1 ( VCAM-1) in human aortic endothelial cells (HAEC). Paper-14386268. ICAM-1 was strongly expressed on endothelial cells as well as on fibroblasts and infiltrating leukocytes while the expression of VCAM-1, similar in its distribution, was much weaker. Paper-275489. Interferon enhances tumor necrosis factor- induced vascular cell adhesion molecule 1 ( CD106) expression in human endothelial cells by an interferon-related factor 1-dependent pathway. Paper-1465781. These data suggest that NF-kappaB plays a key role in low shear- induced VCAM-1 expression and that pathways mediating low shear- and cytokine-induced EC-Mn adhesion may be differentially regulated. Paper-1852745. These results suggest that IL-4- induced oxidative stress upregulates the expression of VCAM-1 gene in HUVEC at transcriptional levels via activation of SP-1 transcription factor. Paper-8691034. TBP I completely abolished TNF-induced IL-6 production and E-selectin induction, while it partially inhibited TNF- induced IL-8 production and up-regulation of ICAM-1 and VCAM-1. Paper-1075633. Involvement of MAPKs and NF-kappaB in tumor necrosis factor alpha- induced vascular cell adhesion molecule 1 expression in human rheumatoid arthritis synovial fibroblasts. Paper-14204675. HGF- mediated inhibition of VEGF-inducible VCAM-1 expression and monocyte adhesion was reversed by overexpression of constitutively active phosphorylation-resistant triple mutant (TM)-FKHR. Paper-13051786. In this study, we show that down-regulation of VCAM-1 by the chemotherapeutic agent etoposide ( VP-16) is associated with altered cellular localization of NF-kappaB. Paper-8793644. Hepatocyte growth factor suppresses vascular endothelial growth factor- induced expression of endothelial ICAM-1 and VCAM-1 by inhibiting the nuclear factor-kappaB pathway. Paper-10791313. PD 144795 treatment markedly inhibited the TNF- induced cell expression of vascular cell adhesion molecule-1 ( VCAM-1) and intercellular adhesion molecule-1 ( ICAM-1) protein and mRNA. Paper-345013. However, adenoviral-mediated expression of catalase only partially inhibited TNF-alpha- induced E-selectin gene expression and had no effect on VCAM-1 and ICAM-1 gene expression. Paper-9676674. This in vitro SAA-enriched HDL(3) inhibited the TNF-alpha- induced expression of VCAM-1 in HUVECs in a concentration dependent manner, which was identical to that of the unmodified HDL(3). Paper-8729395. Furthermore, UTP induced VCAM-1 expression in human 1321N1 astrocytoma cell transfectants expressing the recombinant P2Y2 receptor, whereas vector-transfected control cells did not respond to UTP. Paper-9779916. Studies exploring the underlying mechanism of C1INH- mediated suppression in VCAM-1 expression were related to reduction of NF-kappaB activation and nuclear translocation in an IkappaBalpha-dependent manner. Paper-13270629. Pro alpha1 in combination with TGF-beta1 showed no significant effects on ELAM-1 expression, but antagonized the TGF-beta1- induced decrease of ICAM-1 and VCAM-1 expression on activated HUVECs. Paper-1736495. We conclude that adenosine binding to A(2A)AR counteracts stimulation of neutrophil CD49d integrin expression and neutrophil binding to VCAM-1 via a cAMP/PKA-mediated pathway. Paper-10253331. Eotaxin upregulated the expression of ICAM-1 and VCAM-1 on human nasal mucosal microvascular endothelial cells (HMMEC), but not human umbilical vein endothelial cells (HUVEC). Paper-1267313. Thus, VCAM-1 gene expression appeared to be mediated by NF-kappa b in cardiac myocytes, and this cardiac myocyte VCAM-1 may be involved in cardiac inflammatory disorders. Paper-1324810. PAR2-driven upregulation of VCAM-1 cell surface expression and the release of IL-8 and G-CSF from bronchial fibroblasts may be important in promoting neutrophilic airways inflammation. Paper-12041460. In contrast, vanadate differentially affected TNF alpha-induced expression of these molecules with maximal E-selectin and ICAM-1 expression being slightly enhanced and VCAM-1 expression dose-dependently reduced. Paper-831328. Pretreatment with FP (10(-11) M to about 10(-7) M, 24 h) inhibited TNF-alpha- induced VCAM-1 mRNA expression in BEAS-2B in a dose-dependent manner, but did not inhibit expression of ICAM-1 mRNA. Paper-1824393. Induction of VCAM-1 expression was inhibited by adding neutralizing antibodies against IL-4, whereas IL-6 production and ICAM-1 expression were inhibited by anti- interferon-gamma ( IFN-gamma) antibodies. Paper-300533. Tanshinone I dose dependently inhibited ICAM-1 and VCAM-1 expressions in human umbilical vein endothelial cells (HUVECs) that were stimulated with TNF-alpha for 6 h. Paper-12955274. Here, the roles of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB ( NF-kappaB) pathways for LPS- induced vascular cell adhesion molecule (VCAM)-1 expression were investigated in HTSMCs. Paper-13193892. The anti-inflammatory and (perhaps) antiatherogenic properties of butyrate may partly be attributed to an effect on activation of NF-kappaB and PPARalpha and to the associated expression of VCAM-1 and ICAM-1. Paper-10548706. Additionally, we have shown that P2Y2R activation up-regulates vascular cell adhesion molecule-1 ( VCAM-1) expression in endothelial cells leading to the binding of monocytes. Paper-12488473. Transient transfection of bovine aortic ECs with a VCAM-1 promoter construct revealed that MCC-555 inhibited TNF-alpha- induced VCAM-1 promoter activity. Paper-11508609. Tumor necrosis factor-alpha ( TNF-alpha) induced both VCAM-1 and ICAM-1 expression in human umbilical vein endothelial cells (HUVECs; ED50 approximately 300 and 30 U/ml, respectively). Paper-1936555. The inducible endothelial adhesion molecules, E-selectin, VCAM-1/ alpha 4 beta 1 and vitronectin receptor have been reported to mediate attachment of cancer cells to IL-1-treated endothelial cells. Paper-8230619. 3. Genistein inhibited VCAM-1 expression induced by incubation of HUVEC for 24 h with TNF alpha or IL-1 alpha whereas it did not affect ICAM-1 expression induced by 24 h incubation with either of these cytokines. Paper-831328. Finally, IL-18- induced cell surface VCAM-1 expression was inhibited by treatment with AS ODNs to c-Src, IRAK, PI3-kinase, and ERK1/2 by 57, 43, 41, and 32% compared with control sense ODN treatment, respectively. Paper-9170419. Interleukin-4 ( IL-4) and IL-13 bind to a shared heterodimeric complex on endothelial cells mediating vascular cell adhesion molecule-1 induction in the absence of the common gamma chain. Paper-557295. CONCLUSIONS: PPARgamma activators inhibit expression of VCAM-1 and ICAM-1 in activated endothelial cells and significantly reduce monocyte/macrophage homing to atherosclerotic plaques. Paper-2086817. Our study demonstrated that arsenite pretreatment potentiated the TNF-alpha- induced VCAM-1 expression with up-regulations of both activator protein-1 ( AP-1) and nuclear factor-kappaB ( NF-kappaB). Paper-11156986. However, anti- VCAM-1 antibody failed to clock melanoma cell binding to PMA or IL-1 alpha- stimulated HDMEC and only partially inhibited melanoma cell binding to TNF alpha-stimulated HDMEC. Paper-7208858. Knockdown of CD14 attenuated LPS- mediated up-regulation of ICAM-1 and VCAM-1 mRNA and protein, and it mitigated the effects of GPx-1 deficiency on LPS-induced adhesion molecule expression. Paper-15171898. P2Y2 nucleotide receptor activation up-regulates vascular cell adhesion molecule-1 [corrected] expression and enhances lymphocyte adherence to a human submandibular gland cell line. Paper-12488473. IL-18 requires NF kappa B as well as PI 3-kinase to induce VCAM-1 on RA synovial fibroblasts, suggesting that there may be two distinct pathways in IL-18-induced adhesion molecule expression. Paper-8960423. These results suggest that VEGF- stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activation with PI 3'-kinase-mediated suppression, but was independent of nitric oxide and MEK. Paper-8952800. Prior activation with phorbol 12-myristate 13-acetate (PMA) significantly increased the ability of T cells to up-regulate endothelial ICAM-1 and also induced the expression of both ELAM-1 and VCAM-1. Paper-6873810. CONCLUSIONS: Our findings provide the first evidence that apoCIII increases VCAM-1 and ICAM-1 expression in ECs by activating PKCbeta and NF-kappaB, suggesting a novel mechanism for EC activation induced by dyslipidemia. Paper-12083617. We therefore studied whether IL-13 regulates VCAM-1 in human osteoblastic cells since these cells express RANKL, the major osteoclastogenic factor and osteoclast precursors are found adjacent to osteoblasts. Paper-10018473. The inhibitory effect of SIN-1 was abolished in the presence of a NO scavenger haemoglobin, while addition of 8-bromo-cGMP showed no significant effect on IL-1 beta- induced ICAM-1 or VCAM-1 expression. Paper-1046992. CONCLUSIONS AND IMPLICATIONS: Down-regulation of VCAM and E-selectin expression induced by CORM-3 was independent of HO-1 up-regulation and was predominantly due to inhibition of sustained NF-kappaB activation. Paper-13887462. Here, the roles of mitogen-activated protein kinases (MAPKs) and NF-kappaB in TNF-alpha- induced expression of vascular cell adhesion molecule (VCAM)-1 were investigated in human tracheal smooth muscle cells (HTSMCs). Paper-11388102. On the other hand stimulation of c-met receptor with HGF leads to enhanced integrin- mediated adhesion of activated B cells to vascular cell adhesion molecule ( VCAM-1) and fibronectin. Paper-8727306. During S phase transit, adhesion to Fn was transiently increased while binding to VCAM-1 was reversibly decreased, after which adhesion to both ligands returned to baseline levels with cell cycle completion. Paper-9574241. RESULTS: Intradermal injection of IL-4 induced the expression of vascular cell adhesion molecule-1 ( VCAM-1) on cutaneous vascular endothelium that was present at 8 hr and persisted out to 24 h post injection. Paper-767254. The addition of lacidipine to human umbilical vein endothelial cells significantly reduced the expression of ICAM-1, VCAM-1 and E-selectin induced by TNF-alpha alone or with oxidized LDL ( P < 0.001). Paper-1356688. The considered PPARdelta activator GW501516 and the considered PPARalpha activator fenofibrate also inhibited TNF-alpha- induced VCAM-1 expression, whereas pioglitazone and rosiglitazone did not. Paper-11508609. Vascular cell adhesion molecule-1 ( CD106) is cleaved by neutrophil proteases in the bone marrow following hematopoietic progenitor cell mobilization by granulocyte colony-stimulating factor. Paper-9054961. Both granule proteins and the supernatants of eosinophils cultured with recombinant soluble ICAM-1 induced expression of ICAM-1 and VCAM-1 on endothelial cells, with the latter showing a more prominant increase. Paper-1846483. Our investigation revealed that, by depleting GSH, arsenite attenuated the TNF-alpha- induced VCAM-1 expression as well as a potentiation of AP-1 and an attenuation of NF-kappaB activations by TNF-alpha. Paper-11156986. The expression of LTA-induced E-selectin, ICAM-1, and VCAM-1 in LEC is suppressed by anti-TLR2 but not by anti- TLR4 and is also suppressed by TLR2-specific short interfering RNA (siRNA) but not by siRNA for TLR4. Paper-12944639. Additionally, DNA-PK activity appeared to increase the association between p50/ p50 and p50/p65 NF-κB dimers upon binding to DNA and after binding of p50 NF-κB to the VCAM-1 promoter. Paper-15566594. In addition, GFAT overexpression activated the VCAM-1 promoter (2.25-fold), with further augmentation by high glucose and abrogation by inhibitors of GFAT, NF-kappaB, and O-glycosylation. Paper-9414494. The cytokine transforming growth factor-beta ( TGF-beta) at 2.0 ng/mL inhibited basal VCAM-1 expression by 84 +/- 8% and the induction by TNF-alpha by between 56 +/- 16% and 77 +/- 15% depending on the dose of TNF. Paper-280956. Finally, in synchronized progenitor cells executing a first cell cycle ex vivo, a reversible increase in Fn binding was associated with a reversible decrease in adhesion to vascular cell-adhesion molecule (VCAM)-1. Paper-9963915. Pretreatment of cultured human ECs with the PPARalpha activators fenofibrate or WY14643 inhibited TNF-alpha- induced VCAM-1 in a time- and concentration-dependent manner, an effect not seen with PPARgamma activators. Paper-1892647. The present study demonstrates that activation of the P2Y2R in dispersed cell aggregates from rat submandibular gland (SMG) and in human submandibular gland ductal cells (HSG) up-regulates the expression of VCAM-1. Paper-12488473. The CD81 effect was dependent on both intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 ( VCAM-1), as it was abolished in the presence of a mixture of anti-ICAM-1 and anti- VCAM-1 antibodies. Paper-13495630. Coincubation of neutrophils with alpha-Toc and pretreatment of HUVEC with alpha-Toc significantly reduced PAF-induced CD11b/ CD18 expression and IL-1 beta- induced upregulation of ICAM-1 and VCAM-1, respectively. Paper-1380975. Electrophoretic mobility shift assays revealed that cilostazol repressed TNF-alpha- induced increase in binding of the transcription nuclear factor-kappaB ( NF-kappaB) to its recognition site of VCAM-1 promoter. Paper-9043292. CRP- induced VCAM-1 mRNA expression and this induction was inhibited by protein kinase C (PKC) inhibitors, p38 mitogen-activated protein kinase ( MAPK) inhibitor, and tyrosine kinase inhibitors. Paper-11398387. TNF alpha and LPS- mediated transcriptional activation of the human VCAM-1 promoter through NF-kappa B-like DNA enhancer elements and associated NF-kappa B-like DNA binding proteins was inhibited by PDTC. Paper-7872260. TNF-alpha- enhanced expression of VCAM-1 protein and mRNA as well as phosphorylation of p42/p44 MAPK, p38, and JNK were significantly attenuated by inhibitors of MEK1/2 (U0126), p38 (SB202190), and JNK (SP600125). Paper-11388102. Additionally, silencing of PTEN with specific siRNA showed significant increase of phosphor-Akt compared with TNF-α alone treated ECs. siPTEN significantly upregulated VCAM-1 but was indifferent to ICAM-1 in TNF-α-treated cells. Paper-15440646. 5. Taken together, these data demonstrate that magnolol inhibits TNF-alpha- induced nuclear translocation of NF-kappa B p65 and thereby suppresses expression of VCAM-1, resulting in reduced adhesion of leukocytes. Paper-9354087. Experiments performed using epithelial cells cultured from renal tubules show that VCAM-1 is up-regulated by addition of the inflammatory cytokines tumour necrosis factor-alpha ( TNF-alpha) and interferon-gamma ( IFN-gamma). Paper-7585573. As IL-4 treatment of HUVEC enhanced the intracellular oxidizing potential, as indicated by an increase in 2',7'-dichlorofluorescein (DCF) fluorescence, we studied the effect of antioxidants on IL-4- induced VCAM-1 expression. Paper-8691034. Instead it inhibited VEGF- induced leukocyte-endothelial cell interactions and the endothelial expression of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1). Paper-10791313. It has been concluded that the presence of SAA in HDL has no effect on the ability of these lipoproteins either to inhibit the expression of VCAM-1 in endothelial cells or to bind to proteins on the endothelial cell surface. Paper-8729395. ICAM-1, expressed on the surface of 24-h IFN-gamma- activated HUVECs pretreated with an anti- VCAM-1 mAb to eliminate any VCAM-1-dependent contribution, did not support T cell adhesion under shear conditions. Paper-874987. C-reactive protein activates the nuclear factor-kappaB pathway and induces vascular cell adhesion molecule-1 expression through CD32 in human umbilical vein endothelial cells and aortic endothelial cells. Paper-11308432. In vitro data from brain endothelial cell cultures, provide the first evidence of a role of peroxisome proliferator-activated receptors gamma ( PPARgamma) in WIN55,212-2- induced downregulation of VCAM-1. Paper-13524352. Human immunodeficiency virus-1- tat protein induces the cell surface expression of endothelial leukocyte adhesion molecule-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 in human endothelial cells. Paper-1145882. In addition, cornuside suppressed the expression levels of endothelial cell adhesion molecules including intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) induced by TNF-alpha. Paper-13429484. Cells with marked depletion of cytoplasmic GSH, but with an intact pool of mitochondrial GSH, only slightly enhanced TNF-alpha- induced E-selectin and vascular cell adhesion molecule-1 ( VCAM-1) expression, compared with the control. Paper-2025384. Electrophoretic mobility shift assays of the VCAM-1 promoter demonstrated that hyperosmotic medium suppressed IL-1beta- or TNF-alpha- activated binding activities of IRF-1, but not NF-kappaB, to their respective sites. Paper-9509686. These results suggest that HDL down-regulates the expression of VCAM-1 gene in TNF-alpha- activated HUVECs at transcriptional levels via blunted translocation and transactivation of NF-kappaB and AP-1 transcription factors. Paper-10141913. METHODS: ICAM-1, VCAM-1, and ELAM-1 were analyzed in 20 pancreatic cancer specimens and 20 normal pancreatic tissues. mRNA expression encoding ICAM-, VCAM-1, and ELAM-1 was assessed with Northern blot analysis. Paper-9363879. Based on our findings, we suggest that Nrf2-dependent HO-1 expression induced by HA inhibits MCP-1 secretion, VCAM-1 expression and NF-kappaB activation associated with vascular injury and inflammation in atherosclerosis. Paper-12137231. We demonstrate that the PTK inhibitors herbimycin A or genistein suppress induction of endothelial VCAM-1 and E-selectin, as well as subsequent monocytic cell adhesion to endothelial cells stimulated by TNF. Paper-679428. Our study here provides the information of decrease effect of mER- mediated estrogen through Ca2+ and ERK1/2, p38 MAPK signaling pathway on nicotine- stimulated expression of surface/soluble VCAM-1 and E-selectin in HUVECs. Paper-11827197. Incubation with recombinant human CRP (10 microg/mL) for 24 hours induced an approximately 10-fold increase in expression of ICAM-1 and a significant expression of VCAM-1, whereas a 6-hour incubation induced significant E-selectin expression. Paper-8652005. Here we examined the mechanisms underlying VEGF- stimulated expression of intercellular adhesion molecule 1 ( ICAM-1), vascular cell adhesion molecule 1 ( VCAM-1), and E-selectin in human umbilical vein endothelial cells. Paper-8952800. In contrast to the synergistic effect of IL-13 and tumour necrosis factor-alpha ( TNF-alpha) on endothelial vascular cell adhesion molecule-1 ( VCAM-1) surface expression, TNF-alpha- induced secretion of MCP-1 is not augmented by IL-13. Paper-1154446. In vitro adhesion assays showed that SR-PSOX/ CXCL16 induced adhesion of activated CD8+ T cells to vascular cell adhesion molecule-1 ( VCAM-1) through very late antigen-4 (VLA-4) activation. Paper-10210029. Transient transfection experiments and chromatin immunoprecipitation assays revealed that NOR1 induces VCAM-1 promoter activity by binding to a canonical response element for NR4A receptors in the VCAM-1 promoter. Paper-15372586. Docosahexaenoic acid selectively attenuates induction of vascular cell adhesion molecule-1 and subsequent monocytic cell adhesion to human endothelial cells stimulated by tumor necrosis factor-alpha. Paper-231695. Here, the roles of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB ( NF-kappaB) pathways for IL-1beta- induced vascular cell adhesion molecule (VCAM)-1 expression were investigated in human tracheal smooth muscle cells (HTSMC). Paper-11101696. Here, we show that LPS increased VCAM-1 expression and adhesiveness of HTSMCs through AP-1, since pretreatment with an AP-1 inhibitor tanshinone attenuated LPS- induced VCAM-1 expression and leukocytes adhesion. Paper-13837505. Cotransfection assays in P19 embryonal carcinoma cells revealed that IRF-1 synergized with p50/p65 NF-kappa B to activate the VCAM1 promoter or heterologous promoter constructs bearing isolated VCAM1 NF-kappa B and IRF binding motifs. Paper-218072. At pathophysiological/pharmacological concentrations (10(-9)-10(-7) mol/L), insulin selectively induced VCAM-1 expression and potentiated the effects of TNF-alpha andLPS, effects reverted by the proteasome inhibitor lactacystin. Paper-12912812. Our results show that treatment of EC with HIV- tat induces the cell surface expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial leukocyte adhesion molecule-1 in a time- and dose-dependent manner. Paper-1145882. On the other hand, the TNF-alpha- induced VCAM-1 expression could be completely abolished by inhibition of AP-1 or NF-kappaB activity, suggesting that activation of both AP-1 and NF-kappaB was necessary for VCAM-1 expression. Paper-11156986. Together, these findings indicate that signaling via PKCdelta- p38 kinase- linked cascade specifically induces expression of VCAM-1 in lung epithelium in response to TNF-alpha and that this effect is both functionally and clinically significant. Paper-10760104. Moreover, we found that depletion of GSH would also attenuate the TNF-alpha- induced VCAM-1 expression with a down-regulation of the TNF-alpha- induced NF-kappaB activation and without significant effect on AP-1. Paper-11156986. The preoperative HDL(3) and postoperative, SAA-enriched HDL(3) were identical in terms of their ability to inhibit the tumour necrosis factor-alpha (TNF-alpha)- induced expression of VCAM-1 in human umbilical vein endothelial cells (HUVECs). Paper-8729395. The Cd-induced VCAM-1 expression was significantly suppressed by either a specific p38 mitogen-activated protein kinase ( MAPK) inhibitor (SB202190) or a JNK inhibitor (SP600125), but not by an ERK inhibitor (U0126). Paper-13893162. The IL-1 beta- induced expression of intercellular adhesion molecule 1 ( ICAM-1), vascular cell adhesion molecule 1 ( VCAM-1) and E-selectin 1 (ELAM-1) on SMCs was examined by reverse transcription/ polymerase chain reaction ( RT/PCR). Paper-340687. The involvement of p42/ p44 MAPK and p38 in these responses was further confirmed by that transfection with small interference RNAs (siRNA) direct against MEK, p42, and p38 significantly attenuated LPS- induced VCAM-1 expression. Paper-13193892. These findings reveal for the first time that TNF stimulation of adhesion molecules ICAM-1 and VCAM-1 in human endothelial cells occurs through the TNFR1 subtype and is mediated by the NF-kappaB pathway, but not the ERK, p38MAPK or JNK kinase pathways. Paper-13193888. The vascular cell adhesion molecule 1 ( VCAM-1) is a 110-kD member of the immunoglobulin gene superfamily expressed on the surface of interleukin 1 beta- or tumor necrosis factor alpha (TNF)-stimulated endothelial cells. Paper-7498953. Moreover, calcium chelator BAPTA, ERK1/2 inhibitor PD98059, p38 inhibitor SB203580 significantly reduced the production of nicotine- activated surface/soluble VCAM-1 and E-selectin and both of the remained levels were no longer regulated by estrogen. Paper-11827197. A flavonoid, 2-(3-amino-phenyl)-8-methoxy-chromene-4-one (PD 098063), markedly inhibited TNF- induced VCAM-1 cell-surface expression in a concentration-dependent fashion with half-maximal inhibition at 19 mumol/L but had no effect on ICAM-1 expression. Paper-831441. Further investigations showed that the expression of ICAM-1, VCAM-1 and chemokines stimulated by IL-27 was differentially regulated by intracellular activation of phosphatidylinositol 3-OH kinase-AKT, c-Jun amino-terminal kinase and Janus kinase pathways. Paper-15417738. These findings highlight a novel AR/ NF-kappaB mediated mechanism for VCAM-1 expression and monocyte adhesion operating in male endothelial cells that may represent an important unrecognized mechanism for the male predisposition to atherosclerosis. Paper-10384941. Two serine proteases, namely, neutrophil elastase and cathepsin G, were identified, which cleave VCAM-1 and are released by neutrophils accumulating in the BM during the course of immobilization induced by G-CSF. Paper-9054961. Deletion or mutation of two Src homology-3-binding sites in the C-terminal tail of the P2Y(2)R or inhibition of Src kinase activity abolished the P2Y(2)R-mediated transactivation of VEGFR-2 and subsequently inhibited UTP- induced VCAM-1 expression. Paper-10534020. In contrast, approximately 20% of the total interacting T cells with 24-h IL-4-treated HUVECs were firmly adherent. mAb blocking experiments revealed that T cell adhesion to IL-4-treated HUVECs is alpha 4- VCAM-1 dependent. Paper-874987. AGE increased mRNA levels of vascular cell adhesion molecule-1 ( VCAM-1) and induced monocyte chemoattractant protein-1 ( MCP-1) production in mesangial cells, both of which were prevented by the treatment with nifedipine, but not amlodipine. Paper-13827256. CONCLUSIONS: These findings indicate that in HCAECs, native TRPC3 proteins form channels that contribute to constitutive and ATP-dependent Ca(2+) influx, and that TRPC3 expression and function are fundamental to support VCAM-1 expression and monocyte binding. Paper-13051784. In endothelial cells, the PPARgamma agonists troglitazone at 100 micromol/L and 15-deoxy-(Delta12,14)-prostaglandin J(2) (15d-PGJ2) at 20 micromol/L markedly attenuated the tumor necrosis factor- induced expression of VCAM-1 and ICAM-1. Paper-2086817. Experiments with recombinant proteins showed that p50/p65 and high-mobility-group I(Y) protein cooperatively facilitated the binding of IRF-1 to the VCAM1 IRF binding site and that IRF-1 physically interacted with p50 and with high-mobility-group I(Y) protein. Paper-218072. Results indicated that the equipotent P2Y2 receptor agonists UTP or ATP (1-100 microm) stimulated the expression of vascular cell adhesion molecule-1 ( VCAM-1) in human coronary artery endothelial cells (HCAEC) in a time- and dose-dependent manner. Paper-9779916. In TNFalpha-stimulated HUVEC, simvastatin decreased VCAM-1 and ICAM-1 mRNA levels, inhibited TNFalpha-induced activation of nuclear factor kappaB ( NF-kappaB) and enhanced expression of peroxisome proliferator-activated receptor alpha ( PPARalpha). Paper-10313650. One and 3 years after transplantation, high ICAM and VCAM expression proved to have a negative effect on kidney function in brain dead and living kidneys, while HO-1 proved to have a strongly positive effect, but only in kidneys from living donors. Paper-11584548. TNF-alpha- induced GRO-alpha and IL-8 were slightly attenuated by DEX treatment (reaches to 89% and 79%, respectively), whereas expressions of IP-10, ICAM-1 and VCAM-1 were significantly enhanced by the same treatment (up to 172%, 152% and 139%, respectively). Paper-14486025. The activating anti- ICAM-3 HP2/19 was also able to specifically enhance the VLA-4- and VLA-5- mediated binding of leukemic T Jurkat cells to VCAM-1, FN40, and FN80, even in the absence of cooccupancy of the CD3-TcR complex. Paper-137487. Subarachnoid hemorrhage could induce increases of NF-kappaB DNA- binding activity and the gene expression levels of TNF-alpha, interleukin (IL)-1 beta, ICAM-1, and vascular cell adhesion molecule (VCAM)-1, which were reduced in the PDTC group. Paper-13400338. CONCLUSION: These data suggested that the effect of puerarin-mediated inhibition of TNF-alpha- induced ICAM-1, VCAM-1 and E-selectin expression is attributed to suppressed NF-kappaB activation on the transcriptional level. Paper-14215437. Finally, TNF-alpha- induced activator protein-1 ( AP-1) and nuclear factor-kappaB ( NF-kappaB) activation and resultant intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) expressions were inhibited by ebselen. Paper-10209480. Binding of the nuclear protein to the vWF AT-rich sequence in mobility shift assays is inhibited by competition with a consensus Oct-1 binding site and with a silencer octamer-like sequence from the vascular cell adhesion molecule-1 ( VCAM-1) promoter. Paper-1537635. Adenovirus-mediated overexpression of RORalpha1 inhibited TNF-alpha- induced VCAM-1 and ICAM-1 expression, and overexpression of a mutant form of RORalpha1 (RORalpha1Delta), which inhibited transcriptional activity of RORalpha1 and RORalpha4, attenuated its inhibition. Paper-11066143. We have used the glutathione peroxidase ( GPx) mimic BXT-51072 to assess the possibility that endogenous hydroperoxides play a role in the tumor necrosis factor-alpha (TNFalpha)- induced expression of ICAM-1 and VCAM-1 by monolayers of human endothelial cells. Paper-1595975. Studies based on cell adhesion to two alternatively spliced forms of VCAM-1 or to chimeric molecules generated from them and intercellular adhesion molecule-1 ( ICAM-1) have demonstrated two VLA-4 binding sites on the predominate form of VCAM-1. Paper-8222273. TNF increased VCAM-1 expression to 4.2 times the vehicle-treated control levels ( P < .05) on HT-29 cells and increased ICAM-1 expression on HT-29, LoVo, and SW-620 cells (8.4, 1.8, and 1.9 times vehicle control levels, respectively; P < .05 in each case). Paper-451448. TNF-alpha- mediated induction of vascular cell adhesion molecule-1 ( VCAM-1) was attenuated by all of these inhibitors, whereas in contrast, stimulation of intercellular adhesion molecule-1 ( ICAM-1) was blocked by MG-132 alone. Paper-12320244. These findings suggest that ICAM-1 or ELAM-1 expression of HUVEC stimulated via TXA2 receptors is augmented by induction of NF-kappaB and AP-1 binding activity through the PKC system, and that VCAM-1 expression is augmented by induction of NF-kappaB binding activity. Paper-1475155. Role for neutral sphingomyelinase-2 in tumor necrosis factor alpha- stimulated expression of vascular cell adhesion molecule-1 ( VCAM) and intercellular adhesion molecule-1 ( ICAM) in lung epithelial cells: p38 MAPK is an upstream regulator of nSMase2. Paper-12395076. CONCLUSIONS: These data provide evidence that APE1/ref-1 in endothelial cells mitigates TNF-alpha- induced monocyte adhesion and expression of vascular cell adhesion molecules, and this anti-adhesive property of APE1/ref-1 is primarily mediated by a NOS-dependent mechanism. Paper-11353586. The implication of AP-1 in LPS- induced VCAM-1 expression was confirmed by animal studies showing that pretreatment of mice with tanshinone attenuated LPS-induced VCAM-1 mRNA expression in airway tissues and accumulation of leukocytes in bronchoalveolar lavage. Paper-13837505. Here, we demonstrate that anti- MT1-MMP monoclonal antibody (mAb) impaired monocyte chemotactic protein-1 (MCP-1)- stimulated monocyte migration on fibronectin ( FN), vascular cell adhesion molecule-1 ( VCAM-1), and intercellular adhesion molecule-1 ( ICAM-1). Paper-10775134. The concentration of CCL2 was analyzed by ELISA, while the expression of cell surface ICAM-1 and VCAM-1 and intracellular phosphorylated p38 MAPK, c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase ( ERK) was assessed using flow cytometry. Paper-12944881. Pretreatment with the inhibitors of PKCs or MAPKs attenuated LPS-stimulated nuclear translocation and VCAM-1 promoter binding abilities of AP-1, which attenuated promoter activity and gene expression of VCAM-1 and the adhesiveness between HTSMCs and leukocytes. Paper-13837505. In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta ( IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC). Paper-7872260. We have recently reported that the human lymphatic endothelium has toll-like receptor 4 (TLR4)- mediated lipopolysaccharide recognition mechanisms that induce the expression of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1). Paper-12944639. First, MT1-MMP clustering was observed at motility- associated membrane protrusions of MCP-1- stimulated monocytes migrating on FN, VCAM-1, or ICAM-1 and at the leading edge, together with profilin, of monocytes transmigrating through activated endothelial cells. Paper-10775134. PDTC or N-acetylcysteine dose dependently reduced TNF- induced VCAM-1 but not ICAM-1 surface protein (also in human umbilical arterial endothelial cells) and mRNA expression (by 70% at 100 mumol/L PDTC) in HUVECs as assessed by flow cytometry and polymerase chain reaction. Paper-134323. Collectively, our results suggest that whereas paxillin is a mechanical regulator of VLA-4 bonds generated in the absence of chemokine signals and low VCAM-1 occupancy, talin 1 is a versatile VLA-4 affinity regulator implicated in both spontaneous and chemokine- triggered rapid adhesions to VCAM-1. Paper-13406965. Immunostaining revealed that MKP-1 is preferentially expressed by ECs in a high-shear, protected region of the mouse aorta and is necessary for suppression of EC activation at this site, because p38 activation and VCAM-1 expression was enhanced by genetic deletion of MKP-1. Paper-12953174. Culture of BEAS-2B cells with tumor necrosis factor (TNF)-alpha or interleukin (IL)-1beta (1 ng/ml) was found to enhance intercellular adhesion molecule-1 ( ICAM-1) expression (several fold) and induce de novo CD106 [ vascular cell adhesion molecule-1 ( VCAM-1)] expression. Paper-1230996. Selective inhibitors of p38 MAPK (SB203580), JNK (SP600125) and ERK (PD98059) could suppress TNF-alpha- induced CCL2 and ICAM-1 expression, while only p38 MAPK and ERK inhibitors could suppress TNF-alpha- induced VCAM-1 expression. Paper-12944881. RESULTS: ICAM-1 cross- linking caused an increase in activation of extracellular regulated kinase (Erk)-1/-2 and Jun N-terminal kinase (JNK)-1/-2. mRNA and protein for VCAM-1 was observed after ICAM-1 cross-linking, and this was abrogated by addition of an upstream inhibitor of Erk-1/-2, PD98059. Paper-8972529. Indeed, in BM precursors, neutralizing anti- IL-15 monoclonal antibody (mAb) inhibits the expression of the gamma c chain and of the chemokine stromal derived factor-1 ( SDF-1) but had no effect on vascular cell adhesion molecule 1 ( VCAM-1) and beta1 integrin adhesion molecule expression. Paper-9781046. The noteworthy increase in protein levels of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) induced by TNF-alpha was significantly decreased after incubation of the cells with 1,25(OH)(2)D(3), this effect not being seen on E-selectin expression. Paper-11806441. Here we investigate the hypothesis that low shear-induced activation of NF-kappaB is responsible for enhanced expression of vascular cell adhesion molecule ( VCAM-1) resulting in augmented endothelial cell-monocyte (EC-Mn) adhesion and that this activation is dependent on intracellular oxidant activity. Paper-1852745. The same agents had no significant effect on the constitutive and TNF- stimulated expression of intercellular adhesion molecule 1 ( ICAM-1), whereas the effect on vascular cell adhesion molecule 1 ( VCAM-1) expression was variable depending on cell culture conditions. Paper-690839. In addition, both p38-alpha MAPK and nSMase2 were implicated in the TNF-alpha- stimulated up-regulation of the adhesion proteins vascular cell adhesion molecule-1 ( VCAM) and intercellular adhesion molecule-1 ( ICAM), but this was largely independent of NF-kappaB activation. Paper-12395076. In parallel, DHA inhibited TNF-alpha- stimulated monocytic U937 cell adhesion to HUVECs but did not affect TNF-alpha- or interferon gamma- induced expression of intercellular adhesion molecule-1 and endothelial leukocyte adhesion molecule-1 or VCAM-1 induction by interleukin-1 beta. Paper-231695. 2. Pretreatment of HAECs with magnolol (5 microM) significantly suppressed the TNF-alpha- induced expression of vascular cell adhesion molecule-1 ( VCAM-1) (64.8+/-1.9%), but had no effect on the expression of intercellular cell adhesion molecule-1 and endothelial cell selectin. Paper-9354087. We have previously shown that VCAM-1 expression is induced on human umbilical vein EC (HUVEC) by both tumor necrosis factor alpha ( TNF-alpha) and interleukin-1 alpha ( IL-1 alpha), whereas on human dermal microvascular EC (HDMEC) only TNF alpha results in VCAM-1 expression. Paper-462690. METHODS AND RESULTS: We demonstrate that 15d-PGJ2 induced RORalpha1 and RORalpha4 expression and inhibited TNF-alpha- induced vascular cell adhesion molecule-1 ( VCAM-1) and intercellular adhesion molecule-1 ( ICAM-1) expression in human umbilical vein endothelial cells (HUVECs). Paper-11066143. Stimulation of human umbilical vein endothelial cells (HUVECs) with TNF-alpha resulted in the increase of ICAM-1 and VCAM-1 expressions, while pretreatment with the three components completely inhibited VCAM-1 expression in a dose-dependent manner but had no effect on ICAM-1 expression. Paper-14304350. Only trace amounts of VCAM-1 mRNA or protein were constitutively expressed on dermal fibroblasts but both were rapidly (within 4 hr) upregulated by tumour necrosis factor-alpha ( TNF-alpha) and interleukin-1 alpha ( IL-1 alpha) and somewhat slower (20 hr) by interferon-gamma ( IFN-gamma). Paper-790534. The vascular cell adhesion molecule-1 expression in LME cells and leucocyte- function- associated molecule-1 ( LFA-1) expression in HLA-DR15-positive monocytes were notably enhanced after combined culture of LME cells, HLA-DR15-positive monocytes and TRALI-inducing anti-HLA DR15 antibody-positive serum. Paper-13180964. Electrophoretic mobility shift assay showed that in the activated HUVECs HDL substantially inhibited DNA binding activities of transcription factors of nuclear factor-kappaB ( NF-kappaB) and activator protein-1 ( AP-1) that have binding sites in the promoter region of the VCAM-1 gene. Paper-10141913. In addition, 4-OMGA inhibited the promoter activities of ICAM-1 and VCAM-1 and the activity of nuclear factor-kappaB ( NF-kappaB) without affecting cytosolic IkappaB kinase ( IKK) activation, inhibitor of kappaB (IkappaB) phosphorylation and degradation, and nuclear translocation of NF-kappaB. Paper-12301636. In contrast, Ad.N17Rac1 inhibited TNF-alpha- induced NF-kappaB-driven HIV(kappaB)(4)-CAT and p288VCAM-Luc promoter activity, suggesting that N17Rac1 inhibits TNF-alpha- induced VCAM-1, E-selectin, and ICAM-1 through suppressing NF-kappaB-mediated transactivation. Paper-9676674. IL-27 was found to induce significantly higher cell surface expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 and release of inflammatory chemokine IL-6, CCL2, CXCL9, CXCL10 and matrix metalloproteinase-1 of RA-FLS than that of control FLS (all P < 0.05). Paper-15417738. Cell adhesion was reduced 95+/-4% by monoclonal antibodies HP1/2 and HP2/1, which block VLA-4 binding to both VCAM-1 and FN connecting segment-1. mAb HP1/3 preferentially blocked interaction of VLA-4 with FN but not VCAM-1 and decreased adhesion by 30+/-8%. Paper-8358336. Our initial data indicated that blockade of p38 activity by chemical inhibitor SB203580 (SB) at 10 microM moderately inhibited TNF-alpha-induced expression of three types of CAMs; ICAM-1, VCAM-1 and E-selectin, indicating that p38 may be involved in the process. Paper-13008844. In addition, the results suggest that the increased production of MIP-1 further enhances MM cell binding to stromal cells via stimulation of VLA-4- VCAM-1 adhesion, forming a "vicious cycle" between MM cell adhesion to stromal cells and MIP-1 production via VLA-4- VCAM-1 interaction. Paper-13556604. In DCM patients circulating CD34(+) cell populations were significantly increased in comparison to ICM patients and controls. mRNA of SDF-1, SCF, HIF-1a, and VCAM related to glyceraldehyde-3-phosphate dehydrogenase was significantly upregulated in ICM hearts when compared with DCM hearts and controls. Paper-13245911. Thus, we investigated the effect of anthocyanins on the induction of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) by TNF-alpha and the possible molecular mechanisms by which anthocyanins differentially regulate ICAM-1 and VCAM-1 expression. Paper-14132526. Addition of the structurally unrelated NO donors S-nitrosoglutathione (300 microM) or sodium nitroprusside (1 mM) before low shear stress significantly increased cytoplasmic IkappaBalpha and concomitantly reduced NF-kappaB binding activity and kappaB-dependent VCAM-1 promoter activity. Paper-9657197. Transcription of endothelial-leukocyte adhesion molecule-1 (E-selectin or ELAM-1), vascular cell adhesion molecule-1 ( VCAM-1), and intercellular adhesion molecule-1 ( ICAM-1) is induced by the inflammatory cytokines interleukin-1 beta ( IL-1 beta) and tumor necrosis factor-alpha ( TNF alpha). Paper-295405. TNF-alpha stimulated human umbilical vascular endothelial cells (HUVECs) to upregulate the expression of vascular cell adhesion molecule-1 ( VCAM-1), intercellular adhesion molecule-1 ( ICAM-1) and HLA class I molecules in addition to the induction of procoagulant tissue factor production. Paper-8545737. RESULTS: OPG but not OPN stimulated a dose-dependent increase in the expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin by endothelial cells in the presence of TNF-alpha (p<or=0.05) which was reflected by enhanced binding of THP-1 monocytes. Paper-12591937. Taken together, these data demonstrate that ethyl gallate can inhibit cytokine-induced nuclear translocation of NF-kappaB p65 by way of a mechanism independent of I-kappaBalpha degradation and thereby suppress expression of VCAM-1, ICAM-1, and E-selectin, which was associated with reduced adhesion of leukocytes. Paper-1877393. Our results show for the first time that the expression of VCAM-1 on dystrophic muscle vessels induced by exercise controls muscle homing of human CD133(+) stem cells, opening new perspectives for a potential therapy of muscular dystrophy based on the intra-arterial delivery of CD133(+) stem cells. Paper-12256155. NF-kappaB activation was greatly potentiated by increased 15-LO activity in the stably transduced cells, and both VCAM-1 and ICAM-1 were significantly induced in these cells in response to tumor necrosis factor-alpha ( TNF-alpha) and phorbol 12-myristate 13-acetate (PMA) stimulation, as studied by flow cytometry. Paper-11588860. In vitro, synovial fibroblasts exposed to tumour necrosis factor-alpha ( TNF-alpha) in combination with interferon-gamma ( IFN-gamma) showed enhanced expression of VCAM-1, in comparison with fibroblasts from skin and lung and, unlike skin and lung fibroblasts, also expressed DAF and CR2. Paper-1036229. Flow cytometric analysis of the cultured mast cells showed that IL-4 increases the expression of lymphocyte function- associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 ( ICAM-1), but not of very late antigen (VLA) family adhesion molecules or vascular cell adhesion molecule-1 ( VCAM-1). Paper-1006910. HNMEC differed from human umbilical vein endothelila cells in that (1) maximal upregulation of ICAM-1 expression induced by IL-1beta or TNF-alpha required more time (2) TNF-alpha was more potent than IL-1beta in VCAM-1 expression, and (3) dexamethasone inhibited the upregulation of E-selectin expression alone. Paper-1583826. Treatment of IVEC cells with Interleukin-1 beta ( IL-1 beta) at 10 U.ml-1 activates the expression of cell adhesion molecules such as endothelial leucocyte adhesion molecule ( ELAM-1), intercellular adhesion molecule-1 ( ICAM-1), and vascular cell adhesion molecule-1 ( VCAM-1), as observed in primary culture. Paper-7549815. 4-OMGA inhibited the expression of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-alpha ( TNF-alpha), resulting in the suppression of leukocyte adhesion to HUVECs. Paper-12301636. These data demonstrate that (1) blockade of VCAM-1 can abrogate the majority (75+/-12%) of VLA-4-dependent monocyte adhesion on early atherosclerotic endothelia and (2) ILDV peptide interferes with VLA-4 binding to both VCAM-1 and FN and may be useful in limiting monocyte adhesion to atherosclerotic lesions. Paper-8358336. OPA inhibited expression of vascular cell adhesion molecule-1 ( VCAM-1) and intercellular adhesion molecule-1 ( ICAM-1) stimulated by Tumor Necrosis Factor-α (TNF-α) via activation of PPARα. This inhibition of VCAM-1 and ICAM-1 expression decreased adhesion of monocyte-like cells to stimulated endothelial cells. Paper-15888247. BAI down-regulated the expression of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) in human lung epithelial A549 cells stimulated with tumor necrosis factor-alpha: ( TNF-alpha), resulting in the suppression of leukocyte adhesion to lung epithelial A549 cells. Paper-15235794. In electrophoretic mobility shift assays, thrombin-mediated induction of NF-kappaB p65 binding to two NF-kappaB motifs in the upstream promoter region of VCAM-1 was blocked by LY294002 and rottlerin, whereas the inducible binding of GATA-2 to a tandem GATA motif was inhibited by LY294002 and the PKC-zeta peptide inhibitor. Paper-9844475. In this study, we demonstrated that alpha4 integrin affinity for vascular cell adhesion molecule (VCAM)-1 was upregulated rapidly and transiently by chemoattractants and stromal cell-derived factor (SDF)-1alpha and mediated monocyte arrest. alpha4 integrin affinity changes were detected and blocked using soluble VCAM-1/Fc (sVCAM-1/Fc). Paper-8840760. Here, we report that the POU domain transcription factor Oct-1 represses the expression of E-selectin and vascular cell adhesion molecule ( VCAM-1), two cytokine-inducible, NF-kappaB-dependent endothelial-leukocyte adhesion molecules that participate in the leukocyte recruitment phase of the inflammatory response. Paper-13144125. The alpha 4 beta 1 integrin very late activation antigen-4 (VLA-4) has been implicated to play a role in the adhesive interactions between hematopoietic progenitor cells (HPC) and bone marrow stromal cells which express the vascular cell adhesion molecule-1 ( VCAM-1) or produce fibronectin ( FN). Paper-1048961. Expression of membrane-bound (mb) and soluble (s) forms of vascular cell adhesion molecule-1 ( VCAM-1) and intercellular adhesion molecule-1 ( ICAM-1) induced by tumor necrosis factor-alpha ( TNF-alpha) has been measured by enzyme-linked immunosorbent assay in cultured human brain microvessel endothelial cells. Paper-1760815. Withaferin A inhibited the expression of intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) in human lung epithelial A549 cells stimulated with tumor necrosis factor-alpha ( TNF-alpha), resulting in the suppression of leukocyte adhesion to lung epithelial A549 cells. Paper-13712418. Since IL-10 has previously been documented to down-regulate release of IFN-gamma by PBMC, we propose that the IL-10- mediated reduction of IFN-gamma production by PBMC results in enhanced responsiveness of endothelial cells to PBMC-derived IL-4 and IL-13, and thus increased expression of VCAM-1. Paper-1198787. We report here that 17-epiestriol, an estrogen metabolite and a selective estrogen receptor ( ER) beta agonist, is approximately 400x more potent than 17-beta E(2) in suppressing tumor necrosis factor (TNF) alpha- induced VCAM-1 mRNA as well as protein expression in human umbilical vein endothelial cells. Paper-9663189. CONCLUSION: these results suggest that HSPA12B plays an important role in the attenuation of endotoxin- induced cardiac dysfunction and that the mechanisms involve the preserved activation of PI3K/Akt signalling, resulting in attenuation of LPS-increased expression of VCAM-1/ICAM-1 and leucocyte infiltration into the myocardium. Paper-15584794. We found that LPL treatment reversed tumor necrosis factor alpha and very low-density lipoprotein (VLDL)- stimulated endothelial vascular cell adhesion molecule 1 ( VCAM1) induction and VCAM1 promoter responses, thus recapitulating effects reported with synthetic peroxisome proliferator-activated receptor (PPAR) agonists. Paper-9879223. We investigated signaling pathways leading to tumor necrosis factor (TNF) alpha- induced intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression in chondrosarcoma cells, and determined the functional significance of their expression by examining Jurkat T cell adhesion. Paper-9616104. The aim of this study was to analyse the potential roles of protein kinase enzymes in tumour necrosis factor-alpha ( TNF-alpha) and interleukin-1 (IL-1) induced expression of the adhesion molecules intercellular adhesion molecule-1 ( ICAM-1) and vascular cell adhesion molecule-1 ( VCAM-1) on human umbilical vein endothelial cells (HUVEC). Paper-974867. Compounds 1 and 2 inhibited tumor necrosis factor (TNF)-alpha- induced up-regulation of vascular cell adhesion molecule-1 ( VCAM-1) and intercellular adhesion molecule-1 ( ICAM-1), which also prevented adhesion of monocytes to HUVECs, and slightly suppressed the mRNA expression of the inflammation-associated gene interleukin-1beta (IL-1beta). Paper-12596620. METHODS AND RESULTS: We tested the hypothesis that PPARgamma activators inhibit vascular cell adhesion molecule ( VCAM-1) and intercellular adhesion molecule ( ICAM-1) expression in cultured endothelial cells (evaluated by flow cytometry) and homing of monocyte/ macrophages to atherosclerotic plaques in vivo. Paper-2086817. Taken together, it is suggested that the anti-atherogenic effect of cilostazol in cholesterol-fed Ldlr-null mice is ascribed to its property to suppress superoxide and TNF-alpha formation, and thereby reducing NF-kappaB activation/transcription, VCAM-1/ MCP-1 expressions, and monocyte recruitments. Paper-11208933. Inhibition of tumor necrosis factor-alpha-induced VCAM-1 mRNA levels by forskolin was partially due to enhanced degradation of VCAM-1 message, whereas the decay rates of tumor necrosis factor-alpha-induced ICAM-1 message and interleukin-1beta- induced ICAM-1/ VCAM-1 message were not affected by forskolin treatment. Paper-1187323. The aim of this study was to determine circulating levels of adhesion molecules in serum from patients with congenital diaphragmatic hernia (CDH) to investigate the relationship between soluble ICAM-1, ELAM-1, and VCAM-1 liberated by activated vascular endothelium and the development of persistent pulmonary hypertension ( PPH) in patients with CDH. Paper-10257336. The requirement for p50 NF-κB in TNF- induced VCAM-1 expression may be associated with its interaction with and phosphorylation by DNA-PK, which appears to be dominant over the requirement for p65 NF-κB activation. p50 NF-κB binding to its consensus sequence increased its susceptibility to phosphorylation by DNA-PK. Paper-15566594. We demonstrate a rapid and sustained synergistic increase in tyrosine phosphorylation of human pp125FAK in Jurkat T cells after simultaneous (a) triggering of the TCR-CD3 complex, and (b) alpha 4 beta 1 and alpha 5 beta 1 integrin-mediated binding of these cells to immobilized FN or alpha 4 beta 1 integrin- mediated binding to immobilized VCAM-1. Paper-429955. Using a viral model of MS we observed that the cannabinoid agonist WIN55,212-2 administered at the time of virus infection suppresses intercellular adhesion molecule-1 ( ICAM-1), and vascular cell adhesion molecule-1 ( VCAM-1) in brain endothelium, together with a reduction in perivascular CD4+ T lymphocytes infiltrates and microglial responses. Paper-13524352. These synonyms are used for gene VCAM1 (vascular cell adhesion molecule 1): V-CAM 1, VCAM-1, Vascular cell adhesion protein 1, MGC99561, L1CAM, INCAM-100, DKFZp779G2333, CD106. These accession numbers are used for gene VCAM1: Q6NUP8 (UNIPROT__AC), M30257 (NCBI_GENBANK__AC), AK291732 (NCBI_GENBANK__AC), A8K6R7 (UNIPROT__AC). VCAM1 is a homologue of VCAM1 (vascular cell adhesion molecule 1) from Canis lupus familiaris. VCAM1 is a homologue of VCAM1 (vascular cell adhesion molecule 1) from Bos taurus. VCAM1 is a homologue of VCAM1 (vascular cell adhesion molecule 1) from Bos taurus. VCAM1 is a homologue of VCAM1 (vascular cell adhesion molecule 1) from Gallus gallus. VCAM1 is a homologue of Vcam1 (vascular cell adhesion molecule 1) from Mus musculus. VCAM1 is a homologue of Vcam1 (vascular cell adhesion molecule 1) from Rattus norvegicus. VCAM1 is a homologue of vcam1 (vascular cell adhesion molecule 1) from Danio rerio. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.