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So we assumed that AR could regulate FN synthesis. Paper-14155397.
However, inhibition of AR reverses hyperglycemic suppression of RUNX2. Paper-13860225.
The TRE on the AKR1B1 promoter was localized to the -1099/-1028 region. Paper-13839291.
This study demonstrates AR and SDH in substructures of the kidney. Paper-2882250.
Dominant negative OREBP significantly diminished hyperosmotic AR gene induction. Paper-2186244.
EGF alone elicited activation of ERK and induction of AR expression. Paper-8860831.
Aldose reductase and sorbitol dehydrogenase distribution in rat kidney. Paper-2882250.
Autoimmunity in membranous nephropathy targets aldose reductase and SOD2. Paper-14183315.
Our results show that exposure to HG and overexpression AR increase the expression of FN. Paper-14551845.
Zopolrestat, and CP-470,711 were used to inhibit AR and SDH, respectively. Paper-14338388.
The ratio of activity of AR to SDH was found to be nearly 50 to 1 in all substructures. Paper-2882641.
New member of aldose reductase family proteins overexpressed in human hepatocellular carcinoma. Paper-1373589.
It consists of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH). Paper-2882250.
In this study, we explored the role of AR in FN production and possible mechanism involved. Paper-14155397.
Inhibiting wild-type and C299S mutant AKR1B10; a homologue of aldose reductase upregulated in cancers. Paper-14396548.
Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells. Paper-9876912.
We employed a RT-PCR-based strategy to investigate the regulation of mRNA coding for AR and SDH. Paper-1756149.
OBJECTIVE: Aldose reductase ( ALR) is involved in diabetic microvascular damage via the polyol pathway. Paper-15195945.
Inhibition of AR also prevented the BFGF-induced activation of ERK1/2, JNK, and NF-kappaB in HLECs. Paper-13590230.
Osmotic response element is required for the induction of aldose reductase by tumor necrosis factor-alpha. Paper-1790321.
Aldose reductase gene polymorphisms and susceptibility to diabetic nephropathy in Type 1 diabetes mellitus. Paper-2194546.
Expression of ALR1 and ALR2 in placenta is variable with ALR1/ ALR2 ratios ranging from 1:4 to 4:1. Paper-6540263.
In addition, the within-day preservation rate of AR or AHR activity from each tissue was over 95%. Paper-2163357.
Furthermore, AR overexpression greatly increased the levels of phosphorylated PPARalpha and ERK1/2. Paper-12832354.
TonEBP, in turn, drives the expression of aldose reductase ( AR) and urea transporter-A (UT-A). Paper-12396457.
Taken together, TPA augmented the promoter activity of the AR gene via the activation of protein kinase and NF-kappaB. Paper-11181647.
At 600 mosmol/l, AR activity increased to 82.5+/-11.4 U/g protein and SDH activity to 31.5+/-6.0 U/g protein. Paper-10121500.
Thus, when glucose is depleted, the regulation of AR expression by bFGF does not operate. Paper-1077799.
Aldose reductase and sorbitol dehydrogenase distribution in substructures of normal and diabetic rat lens. Paper-2882641.
A similar pattern of AR promoter response was observed between TNF-alpha and osmotically stressed human liver cells. Paper-1790321.
Diabetic retinopathy: Validation study of ALR2, RAGE, iNOS and TNFB gene variants in a south Indian cohort. Paper-15504856.
Similar to AR, ARL-1 can efficiently reduce aliphatic and aromatic aldehydes, and it is less active on hexoses. Paper-1431095.
Aldose reductase is a potent regulator of TGF-β1 induced expression of fibronectin in human mesangial cells. Paper-14555408.
Treatment of neonatal animals with furosemide dramatically reduced expression of TonEBP, AR, and UT-A1. Paper-12396457.
AR protein expression increased severalfold in human liver cells after 1 day of exposure to 100 units/ml TNF-alpha. Paper-1790321.
Structure of aldehyde reductase in ternary complex with a 5-arylidene-2,4-thiazolidinedione aldose reductase inhibitor. Paper-14670645.
The activities and protein levels of AR and SDH were higher in the ovary than in the oviduct and uterus. Paper-10023584.
Hyperglycemia regulates RUNX2 activation and cellular wound healing through the aldose reductase polyol pathway. Paper-13860225.
Interestingly, supply of AOP2 and/or the AR inhibitor fidarestat protected the cells against hyperglycemia-induced death. Paper-10364461.
Role of aldose reductase in TGF-beta1- induced fibronectin synthesis in human mesangial cells. Paper-14155397.
Exposure to TNF-alpha also induced apoptotic cell death, which was attenuated by AR inhibition or antisense ablation. Paper-10488915.
Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Paper-12396457.
During the initiation phase, the intensity of diapause and the levels of AR and SoDH transcripts increased and reached a maximum. Paper-12699402.
Inhibition of AR prevented HNE- or GS-HNE- induced but not GS-DHN- induced up-regulation of COX-2 and PGE(2). Paper-12254317.
Induction of aldose reductase ( AR) was observed in human cells treated with tumor necrosis factor-alpha ( TNF-alpha). Paper-1790321.
These observations suggest that AR is a critical regulator of TNF-alpha-induced apoptotic signaling in endothelial cells. Paper-10488915.
The inhibition of AR also prevents the apoptosis of VECs induced by the tumor necrosis factor-alpha ( TNF-alpha). Paper-9876912.
On the other hand, osmotic stress elicited significant increases in AR mRNA without any effect on SDH mRNA expression. Paper-8821113.
Aldose reductase mediates cytotoxic signals of hyperglycemia and TNF-alpha in human lens epithelial cells. Paper-9707014.
Z+2 allele of ALR2, 13-repeat genotype of iNOS, 15-repeat genotype of TNF-β, genes were associated with susceptibility to DR. Paper-15504856.
We detected specific anti- aldose reductase ( AR) and anti-manganese superoxide dismutase ( SOD2) IgG(4) in sera of patients with MN. Paper-14183315.
Aldose reductase regulates TNF-alpha-induced cell signaling and apoptosis in vascular endothelial cells. Paper-10488915.
Inhibitors of NF-kappaB signaling, lactacystin, and MG132 abolished the AR promoter response to TNF-alpha. Paper-1790321.
3-FS formation was reduced by the AR inhibitor AL 1576, and 3-FF formation was eliminated by the SDH inhibitor CP-166,572. Paper-1655556.
Lowering osmolarity from 600 to 300 mosmol/l, enzyme activity decreased to less than half within 2 ( AR) or 1 ( SDH) day(s). Paper-10121500.
Role of aldose reductase in the high glucose induced expression of fibronectin in human mesangial cells. Paper-14551845.
However, there has been surprisingly little research on the relative abundance of SDH to AR in the tissues affected in diabetes. Paper-8909089.
Further studies are warranted to explore the role of AR in DN and the therapeutic implications by AR inhibitors such as BBR. Paper-12831913.
Aldose reductase and aldehyde reductase were purified to homogeneity from multiple samples of human kidney cortex and medulla. Paper-7744742.
Inhibition of AR by sorbinil or tolrestat prevented TNF-alpha-induced increase in Bax and Bak and the downregulation of Bcl-2. Paper-10488915.
Osmoregulation of aldose reductase and sorbitol dehydrogenase in cultivated interstitial cells of rat renal inner medulla. Paper-10121500.
In conclusion, increased AR activity contributes to retinal oxidative stress and VEGF protein overexpression in early diabetes. Paper-9877035.
This is also the first study to demonstrate that PS is a Nrf2 inducer and AR inhibitor in the AOM-treated colon carcinogenesis model. Paper-15744262.
In the enzyme preparation from rat or human tissues obtained by this method, two active peaks were identified as AR and AHR. Paper-2163357.
Digestion with restriction enzymes and sequencing of the products clearly indicate that the specific mRNA of AR and SDH was amplified. Paper-1756149.
We evaluated their ALR2 selectivity profile against sorbitol dehydrogenase and aldehyde reductase ( ALR1). Paper-15452233.
The estimation of the AR cDNA/ SDH cDNA ratio showed that the relative abundance of SDH to AR differs among tissues. Paper-9382390.
The polyol pathway consists of two enzymes, aldose reductase ( AR) and sorbitol dehydrogenase ( SDH). Paper-9255608.
The expressions of AR and SDH mRNAs in Schwann cells were unaltered by high (30 mM) glucose content in the medium. Paper-8821113.
The gene encoding aldose reductase ( ALR) has been cloned from Leishmania donovani, a protozoan parasite causing visceral leishmaniasis. Paper-13492109.
The bcl-2 mRNA was rapidly downregulated while bax and bclxL gene expression was not altered in both differentiating HL60 and HL60/ ADR cells. Paper-539638.
AR2 but not AR1 mRNA was significantly increased some 11- to 18-fold by hyperosmolarity in several retinal pigment epithelial cell lines. Paper-97174.
Results are featured for three enzymes: triosephosphate isomerase ( TIM), aldose reductase ( AR), and phosphomannose isomerase ( PMI). Paper-9078770.
An increase in AR transcripts was also observed in human liver cells after 3 h of TNF-alpha treatment, reaching a maximum level of 11-fold at 48 h. Paper-1790321.
However, when the concentration of glucose in the culture medium was under 1 g/l, bFGF did not increase the activity of AR. Paper-1077799.
A recent meta-analysis found genetic variation in the ALR gene ( AKR1B1) to be significantly associated with diabetic retinopathy (DR). Paper-15195945.
Interestingly, ARL-1 and AR are overexpressed in some liver cancers, but it is not clear if they contribute to the pathogenesis of this disease. Paper-1431095.
In conclusion, our data support AR and SOD2 as renal antigens of human MN and suggest that oxidative stress may drive glomerular SOD2 expression. Paper-14183315.
In addition, inhibition of AR prevented LPS- induced activation of protein kinases upstream to NF-kappaB activation such as PKC and MAPK in HLECs. Paper-12329110.
Polyol pathway-dependent osmotic and oxidative stresses in aldose reductase-mediated apoptosis in human lens epithelial cells: role of AOP2. Paper-10364461.
Enzyme activities of AR and SDH, which were lower in 20 week old OLETF rats than in LETO rats, were increased in 60 week old OLETF rats. Paper-9055106.
The enzyme activity of AR showed a fourfold increase from cortex to papilla, while SDH-activity dropped from cortex to papilla by a factor of four. Paper-13622254.
The aldose reductase inhibitor zopolrestat partially restored the levels of CAT, CuZnSOD, and GPX mRNA in the patients with nephropathy ( P < 0.05). Paper-9877032.
Localization and physiological implication of aldose reductase and sorbitol dehydrogenase in reproductive tracts and spermatozoa of male rats. Paper-9295156.
Among the three inflammatory cytokines: TNF-alpha, interleukin-1, and interferon-gamma, TNF-alpha (100 units/ml) gave the most induction of AR. Paper-1790321.
Our results show that the four inhibitors follow either uncompetitive or non-competitive inhibition pattern of substrate reduction for ALR1 and ALR2. Paper-13599393.
Ischemic activation of AR was increased in GRX-null hearts but was attenuated in the hearts of cardiospecific GRX transgenic mice. Paper-15364636.
BACKGROUND: The C-106T polymorphism of AKR1B1, which encodes aldose reductase ( AR), was reported to be associated with diabetic nephropathy ( DN). Paper-10119101.
CONCLUSION: We suggested that aldose reductase inhibitor may have preventive effect on diabetic nephropathy by reducing renal VEGF overexpression. Paper-14704687.
Inhibition of flux through this pathway can be blocked through inhibition of either of 2 enzymes, aldose reductase ( AR) or sorbitol dehydrogenase ( SDH). Paper-15249645.
Inhibition of AR abrogated AP-1 DNA binding activity and prevented the activation of caspase-3, JNK, and p38 MAPK in cells stimulated by TNF-alpha. Paper-10488915.
Upon resumption of direct development ( oogenesis, mating and oviposition), the relative abundances of AR and SoDH transcripts decreased to trace levels. Paper-12699402.
These results indicate that different tissues contain varying amounts of AR mRNA and SDH mRNA; that is, each tissue has its own polyol pathway activity. Paper-9382390.
Rat renal expression of mRNA coding for aldose reductase and sorbitol dehydrogenase and its osmotic regulation in inner medullary collecting duct cells. Paper-1756149.
Our results showed that AR could mediate the TGF-beta1- induced FN production, which may associate with AP-1 activation. Paper-14155397.
Although both AR and SDH mRNA were expressed in the Schwann cells, the levels of SDH cDNA were much lower than those of AR cDNA. Paper-8909089.
These results indicate that AR is expressed in astrocytes and that its expression is upregulated by hypertonicity but also by FGFs and EGF. Paper-1077799.
Activation of AR by bradykinin and insulin was reversed upon reduction with dithiothreitol or by inhibiting NOS or PI3K. Paper-14301443.
One focus of asthma pharmacogenetic research has been the beta2-adrenergic receptor gene ( ADR beta 2) and its effect on individual responses to beta agonist therapy. Paper-12600839.
Treatment of VECs with the AR inhibitor, tolrestat, prevented the activation of NF-kappaB and diminished ICAM-1 induction stimulated by TNF-alpha. Paper-9876912.
This protein, which we called ARL-1, consists of 316 amino acids, the same size as AR, and its amino acid sequence is 71% identical to that of AR. Paper-1431095.
METHODS: Seven candidate genes (RAGE, PEDF, AKR1B1, EPO, HTRA1, ICAM and HFE) were chosen based on reported association with DR in the literature. Paper-15531024.
These data indicate that AR plays an important role in the regulation of hepatic PPARalpha phosphorylation and activity and lipid homeostasis. Paper-12832354.
The ADR model demonstrated higher range of motion (ROM), annulus stress, and facet contact pressure at the surgical level compared to the non-modified INT model. Paper-13536086.
Deletion of AR-protected animals from severe neurological deficits and large infarct, whereas similar protection was not observed in mice with SD deficiency. Paper-13350210.
Confocal and immunoelectron microscopy (IEM) showed co-localization of anti- AR and anti- SOD2 with IgG(4) and C5b-9 in electron-dense podocyte immune deposits. Paper-14183315.
The effect of AR inhibition on basic fibroblast growth factor (BFGF)-induced mitogenic signaling in cultured human lens epithelial cells (HLECs) was examined. Paper-13590230.
Allelic and genotypic constitution of 10 polymorphisms ( SNPs) from five genes namely--ADPRT1, AKR1B1, RAGE, GFPT2 and PAI-1 with diabetic CRI was investigated. Paper-15247934.
We also observed a time-dependent induction by D3T of mRNA expression for Cu,ZnSOD, MnSOD, gamma-glutamylcysteine ligase, GR, GSTA1, GSTM1, NQO1, AR, and HO-1. Paper-13692590.
The excess VEGF immunoreactivity and increased MDA and AR activity determined in diabetic retina were significantly attenuated by individual antioxidant treatments. Paper-13283013.
EGF receptor-ERK pathway is the major signaling pathway that mediates upregulation of aldose reductase expression under oxidative stress. Paper-8860831.
Differences in the pattern of AR induction were observed in human liver, lens, and retinal pigment epithelial cells with increasing concentrations of TNF-alpha. Paper-1790321.
Association analysis of ADPRT1, AKR1B1, RAGE, GFPT2 and PAI-1 gene polymorphisms with chronic renal insufficiency among Asian Indians with type-2 diabetes. Paper-15247934.
While AR mRNA is found in most tissues studied, ARL-1 is primarily expressed in the small intestines and in the colon, with a low level of its mRNA in the liver. Paper-1431095.
JM2 cells, with increased ALDH and ALRD and decreased ADH and GST, are much more resistant to the toxic effects of 4-HNE than 7777 cells. Paper-8011264.
Electrophoretic analyses of alcohol dehydrogenase, aldehyde dehydrogenase, aldehyde reductase, aldehyde oxidase and xanthine oxidase from horse tissues. Paper-4544762.
These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. Paper-13560285.
Expression of SPR showed a significant 4-fold increase in PD cases relative to controls, while the expression of AKR1B1 and PTS was significantly decreased in PD cases. Paper-13136535.
The separation of AR and AHR from tissue extracts using an anion-exchange column was followed by chromatographic measurement of the activity in the elute. Paper-2163357.
Treatment with AR inhibitors significantly prevented the lens epithelial cell growth in capsular bags and expression of alpha-SMA, beta-crystallin, and ICAM-1. Paper-13590230.
Immunohistochemical analysis was performed in paraformaldehyde-fixed eye sections by staining with antibodies against iNOS, COX-2, TNF-alpha, NF-kappaB, and AR. Paper-12485930.
Studying the time course of enzyme activity after changing osmolarity from 300 to 600 mosmol/l, we found half maximal stimulation after 2-3 ( AR) or 3 ( SDH) days. Paper-10121500.
This decrease in unprocessed TNF-alpha was prevented by the aldose reductase ( AR) inhibitor sorbinil and AR small interference RNA. Paper-13560285.
RESULTS: Ex vivo addition of AGE-BSA increased AR activity, TGF-beta1 and type IV collagen mRNA levels in both WT and TG glomeruli, with greater rise in TG glomeruli. Paper-10903414.
Several of these genes had previously been associated with cancer, namely inositol 1,4,5-triphosphate 5-phosphatase, vimentin, aldose reductase and elongation factor-1alpha. Paper-10396381.
Aldose reductase regulates hepatic peroxisome proliferator-activated receptor alpha phosphorylation and activity to impact lipid homeostasis. Paper-12832354.
Like SMIT, BGT1 and AR genes, TauT, CDO and CSD genes appear to be tonicity-sensitive genes which can be activated in vivo by hypertonicity in the rat kidney. Paper-8956633.
Expression of aldose reductase and sorbitol dehydrogenase genes in Schwann cells isolated from rat: effects of high glucose and osmotic stress. Paper-8821113.
These results suggest that polymorphisms in the promoter region of the VEGF gene together with the ALR2 may be associated with the pathogenesis of diabetic nephropathy. Paper-9715409.
We note that TIM and AR have similar structures but catalyze different kinds of reactions, whereas TIM and PMI have different structures but catalyze similar reactions. Paper-9078770.
Aldose reductase regulates growth factor- induced cyclooxygenase-2 expression and prostaglandin E2 production in human colon cancer cells. Paper-12254317.
The affinity (Km) of AR for 3-FG is approximately 20-fold better than that for D-glucose, whereas the Km of SDH for 3-FS was fourfold less than for D-sorbitol. Paper-1655556.
Our study revealed that substitutions in the C7 OH group enhanced the potency toward ALR2, while the C6 OH group interferes with ALR1 inhibition activity. Paper-15452233.
We investigated the selectivity-determining features by gradually mapping the residues deviating between the binding pockets of ALR1 and ALR2 into the ALR2 binding pocket. Paper-14451011.
Methylglyoxal metabolism and diabetic complications: roles of aldose reductase, glyoxalase-I, betaine aldehyde dehydrogenase and 2-oxoaldehyde dehydrogenase. Paper-9876887.
In conclusion, our data show that bcl-2 overexpression enhances both tumorigenicity and metastatic potential of MCF7 ADR cells by inducing metastasis-associated properties. Paper-1195706.
Here we report the potency of fibrate-mediated inhibition of the carbonyl reduction catalyzed by wild-type and C299S mutant AKR1B10 and compare it with known AR inhibitors. Paper-14396548.
In this study, we investigated the effects of aldose reductase inhibitor, fidarestat on diabetic nephropathy, and renal VEGF expression in a type 1 diabetic rat model. Paper-14704687.
Postischemic deactivation of cardiac aldose reductase: role of glutathione S-transferase P and glutaredoxin in regeneration of reduced thiols from sulfenic acids. Paper-15364636.
AR also negatively regulates RUNX2-dependent vascular remodeling in an EC wounded monolayer assay, which is reversed by specific AR inhibition in hyperglycemia. Paper-13860225.
These results show that inhibition of AR may be useful to prevented extracellular matrix ( ECM) deposition in diabetic nephropathy, which is regulated by JNK and AKT. Paper-14551845.
Accordingly, neutralizing antibodies against the putative EGFR ligand transforming growth factor-alpha ( TGF-alpha) abolished AR induction during osmotic stress. Paper-13734398.
Analysis of gene expression of aldose reductase and sorbitol dehydrogenase in rat Schwann cells by competitive RT-PCR method using non-homologous DNA standards. Paper-8909089.
In this study, we examined the role of aldose reductase ( AR) in regulating the cytotoxic effects of TNF-alpha on human umbilical vein endothelial cells. Paper-10488915.
C-106T polymorphism of AKR1B1 is associated with diabetic nephropathy and erythrocyte aldose reductase content in Japanese subjects with type 2 diabetes mellitus. Paper-10119101.
These data provide direct evidence that the SMIT, AR, and HSP70 genes are targets of TonEBP, although the potential role of other proteins, such as accessory proteins, cannot be excluded. Paper-9767071.
Aldose reductase ( AR) has emerged as a key contributor to the diabetic nephropathy ( DN), however, the mechanisms by which AR increases DN remain poorly understood. Paper-14551845.
Moreover, AR- induced suppression of PPARalpha activity was attenuated by treatment with an inhibitor for ERK1/2 but not that for phosphoinositide 3-kinase, p38, or JNK. Paper-12832354.
Flux via the polyol pathway, which comprises the enzymes aldose reductase ( AR) and sorbitol dehydrogenase ( SDH), has been implicated in the debilitating complications of diabetes. Paper-6856719.
DNA binding of tonicity-responsive enhancer binding protein ( TonEBP, a transcriptional regulator of AR) paralleled AR mRNA, declining >50% in late HF ( P < 0.025 vs. control). Paper-9173442.
This is mediated through combating oxidative stress of free radicals, improving the energy metabolic state of the cell, and enhancing the activity of G6Pase, GST and AR enzymes. Paper-14334961.
However, unlike AKR1A1 and AKR1B1, both AKR1C1 and AKR1C4 were able to catalyse the oxidation of 1-acenaphthenol and, in addition, AKR1C4 could oxidize di- and tri-hydroxylated bile acids. Paper-2039223.
Thus, euglycemia supports RUNX2 activity and promotes normal microvascular EC migration and wound healing, which are repressed under hyperglycemic conditions through the AR polyol pathway. Paper-13860225.
The AGE-induced enhancement in TGF-beta1 and type IV collagen expression were suppressed by either zopolrestat or transfection with an AR antisense oligonucleotide. Paper-10903414.
Aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) make up the sorbitol pathway, which has been implicated in the pathogenesis of sugar cataracts. Paper-2882641.
The high selectivity of ponalrestat in favour of ALR2 rather than ALR1 suggests that the compound is unlikely to inhibit other enzymes which have less homology with ALR2. Paper-6524729.
In streptozotocin-diabetic mice, AR inhibitor treatment or genetic deficiency of AR resulted in significant dephosphorylation of both PPARalpha and ERK1/2. Paper-12832354.
Expression of aldose reductase, sorbitol dehydrogenase and Na+/myo-inositol and Na+/Cl-/betaine transporter mRNAs in individual cells of the kidney during changes in the diuretic state. Paper-1739702.
Treatment with HG and transfected with plasmid PcDNA3.0- AR, resulted in phosphorylation and activation of ERK, JNK and AKT signaling pathway, and increase the expression of FN. Paper-14551845.
The described combined approach by intra-arterial infusion of ADR and BLM and cytokinetically controlled irradiation was able to produce CR in all treated primary tumors of the head and neck. Paper-4325231.
Our findings suggest that P-gp may be induced by AR over-expression and/or osmotic stress, thus playing a regulatory role in maintaining lenticular osmotic balance in sugar cataract. Paper-12383030.
The contribution of MMP/ EGFR signaling in vivo was confirmed in C57BL/6 mice, in which treatment with GM6001 was associated with reduced AR induction following dehydration. Paper-13734398.
Inhibition of aldose reductase prevents growth factor- induced G1-S phase transition through the AKT/phosphoinositide 3-kinase/ E2F-1 pathway in human colon cancer cells. Paper-14773223.
Inhibitory effects of fidarestat on aldose reductase and aldehyde reductase activity evaluated by a new method using HPLC with post-column spectrophotometric detection. Paper-2163357.
Fidarestat, a newly developed AR inhibitor, and N-acetylcysteine, an antioxidant, completely prevented these deleterious effects of SDH overexpression on pericytes. Paper-9255608.
Setting: The pharmacies in Shiraz, capital of Fars province in Iran. Methods A questionnaire was prepared to investigate knowledge and attitude of pharmacists regarding ADR reporting. Paper-13680839.
The polyol metabolizing pathway, which consists of two enzymes, aldose reductase ( AR) and sorbitol dehydrogenase ( SDH), converts glucose to fructose. Paper-9295156.
Aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) are the enzymes constituting the polyol pathway, an alternate route of glucose metabolism. Paper-8909089.
Sorbitol synthesis is regulated by the enzyme aldose reductase ( AR) and its degradation to fructose is catalyzed by the enzyme sorbitol dehydrogenase ( SDH). Paper-13622254.
We performed this study to determine whether and how AR might influence hepatic peroxisome proliferator-activated receptor alpha ( PPARalpha) activity and lipid metabolism. Paper-12832354.
These effects were significantly attenuated in the presence of BAY11-7082, indicating the involvement of NF-kappaB in the cellular response of AR to oxidative stress and toxic aldehydes. Paper-12989871.
In ALR2, Thr113 (Tyr116 in ALR1) forms electrostatic interactions with the fluorobenzyl moiety of Minalrestat and the 3- and 4-hydroxy groups on the phenyl ring of quercetin. Paper-13599393.
(CA)(n) repeat, Gly82Ser, (CCTTT)(n) repeat and (GT)(n) repeat in ALR2, RAGE, iNOS and TNFB genes respectively were genotyped and their frequencies were analyzed using the relevant statistical tests. Paper-15504856.
AR and AHR activity were expressed as the area under the peak obtained by post-column spectrophotometric detection of the decrease of coenzyme ( NADPH) in each enzyme reaction. Paper-2163357.
In ischemic cardiospecific AR transgenic hearts, AR was co-immunoprecipitated with GSTP, whereas in reperfused hearts, the association of AR with GRX was increased. Paper-15364636.
The RT-PCR system developed in this study may be a useful tool in ascertaining the relative contributions of AR and SDH to the metabolic derangements leading to diabetic complications. Paper-8821113.
For characterization we studied regulation of sorbitol synthesis by aldose reductase ( AR) and degradation by sorbitol dehydrogenase ( SDH) in papillary interstitial cells. Paper-10121500.
Furthermore, hypertonic induction of AR gene was associated with an OREBP-dependent hyperacetylation of histones that spanned the 5' upstream sequences and at least some exons of the gene. Paper-14624052.
The first enzyme in the pathway, aldose reductase ( AR), reduces glucose to sorbitol, which is then converted to fructose by sorbitol dehydrogenase ( SDH). Paper-9927144.
Anion-exchange chromatography of human renal cytosol on Q-Sepharose allowed resolution of AKR1A1, AKR1B1, AKR1C1 and AKR7A2, as identified by substrate specificity and Western blotting. Paper-2039223.
A selective epidermal growth factor ( EGF) receptor kinase inhibitor, tyrphostin AG1478, significantly suppressed the hydrogen peroxide (H2O2)-induced increase in AR mRNA and enzyme activity. Paper-8860831.
Expression and activities of AR and SDH were significantly higher in aged vs. young hearts, and induction of ischemia further increased AR and SDH activity in the aged hearts. Paper-16106991.
Many of the complications of diabetes seem to be due to aldose reductase ( aldehyde reductase 2, ALR2) catalysing the increased conversion of glucose to sorbitol. Paper-7016560.
Following antidiuresis, the mRNA levels of TauT, CDO, CSD, SMIT, BGT1 and AR were all similarly increased in the papilla when compared with levels in rats submitted to a chronic diuresis. Paper-8956633.
Comorbid LUTS and ED are treated with an alpha1- AR antagonist and a PDE-5; however, this combination must be used with caution because of vasodilatory adverse events associated with both classes of drugs. Paper-12355086.
More importantly, inhibition of AR prevented the EGF- and bFGF- induced activation of phosphoinositide 3-kinase/ AKT and reactive oxygen species generation in colon cancer cells. Paper-14773223.
We along with others have recently found that SDH activity, the second step in the polyol pathway, might make a greater contribution to the etiology of diabetic retinopathy than does the first step involving AR. Paper-9905376.
CONCLUSION: The TT genotype of the C-106T polymorphism of AKR1B1 increases the risk for DN in Japanese subjects with type 2 diabetes mellitus, which could be linked in part to greater expression of AR. Paper-10119101.
We have reported on the SPR-unrelated novel biosynthetic pathway from PPH(4) to BH(4) (salvage pathway II) in which 3alpha-hydroxysteroid dehydrogenase type 2 and aldose reductase work in concert. Paper-14545537.
Inhibition of AR in VSMC also prevented the activation of NF-kappa B by basic fibroblast growth factor ( bFGF), angiotensin-II ( Ang-II), and platelet-derived growth factor (PDGF-AB). Paper-9169309.
AIMS: To investigate association and linkage between DNA sequence variants in the aldose reductase ( AR) gene on chromosome 7q35 and diabetic nephropathy ( DN) in Type 1 diabetes mellitus. Paper-2194546.
Refining the admission interview process to obtain accurate medication information--including alternative and OTC drugs--will help to decrease the incidence of drug interactions and ADR in the acute care setting. Paper-9425981.
These results indicate an obligatory requirement of AR activity in the transduction of intracellular signaling initiated by the ligation of the TNF-alpha receptors leading to the activation of NF-kappaB. Paper-9876912.
In early HF, decreased AR occurs due to a translational or posttranslational mechanism, whereas in late HF reduced TonEBP transcriptional activation and AR downregulation contribute significantly. Paper-9173442.
In PTEC no regulation of aldehyde reductase and aldose reductase by atorvastatin could be measured, while the expression of small intestine reductase was reduced by 37% compared with control medium ( P < 0.05). Paper-13813497.
The identified protein is designated as RSOR because it is renal-specific with properties of an oxido-reductase, and like ALR2 it may be relevant in the renal complications of diabetes mellitus. Paper-8380730.
Small interfering RNA (siRNA) against p65 or BAY11-7082, an inhibitor of NF-kappaB, significantly suppressed the curcumin and/or Nrf2-induced increase in expression levels and promoter activity of the AR gene. Paper-12989871.
Among pharmacologic options, alpha1-adrenergic receptor ( alpha1- AR) antagonists provide effective treatment with a low risk of sexual side-effects; some of these drugs have been reported to improve sexual function. Paper-12355086.
CONCLUSIONS: Association between DN and two DNA sequence variants in the promoter region of the AR gene implicates the polyol pathway in the development of kidney complications in Type 1 diabetes mellitus. Paper-2194546.
The LPS-induced increased expression of AR, TNF-alpha, iNOS, and COX-2 proteins in the ciliary body, corneal epithelium, and retinal wall was also significantly inhibited by zopolrestat. Paper-12485930.
The present results suggest that AKR1B1 and CTSH may be good markers for prediction of sensitivity to certain drugs and that our panel of 39 cell lines has the potential to identify candidate predictive marker genes. Paper-10197501.
The TPA-induced increase in mRNA level and promoter activity of the AR gene was significantly attenuated in the presence of an inhibitor of protein kinase C, tyrosine kinase, or nuclear factor kappaB ( NF-kappaB). Paper-11181647.
Diabetic retinopathy in Euro-Brazilian type 2 diabetic patients: relationship with polymorphisms in the aldose reductase, the plasminogen activator inhibitor-1 and the methylenetetrahydrofolate reductase genes. Paper-9961816.
The enzymatic activities, expression, and localization of AR and SDH were studied in reproductive tracts and spermatozoa of male rats by immunohistochemistry, Western blotting, and enzyme assays. Paper-9295156.
RESULTS: In HUVEC, atorvastatin reduces the expression of aldehyde reductase and aldose reductase compared with control medium (-20% and -12% respectively, P < 0.05), while small intestine reductase is not expressed. Paper-13813497.
The expression of AR, FN and c-Jun proteins were analyzed by Western blot and the activity of activator protein-1 ( AP-1) was assessed by electrophoretic mobility shift assay (EMSA). Paper-14155397.
Enzymes capable of these reactions have been referred to as aldehyde reductase ( ALR1), aldose reductase ( ALR2), and carbonyl reductase (ALR3); however, ALR3 is not a member of the AKR superfamily. Paper-1173243.
Myocardial function, substrate flux via AR and SDH, and tissue lactate:pyruvate (L/ P) ratio (a measure of cytosolic NADH/ NAD+), and lactate dehydrogenase (LDH) release (a marker of IR injury) were measured. Paper-14338388.
The abundance of AR compared with SDH suggests that it also plays an additional role in the reproductive system, which might include a source of reducing power and protection against toxic carbonyl compounds. Paper-10023584.
We investigated the role of polyol pathway enzymes aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) in mediating injury due to ischemia-reperfusion (IR) in Type 2 diabetic BBZ rat hearts. Paper-14338388.
We have found, either by northern blot or quantitative reverse transcriptase-PCR analysis, that the expression of three genes, Csn2, Aldose reductase and Brf1, is lost at different ratios in tumors of different origins. Paper-14383645.
METHODS: Interstitial cells were isolated from rat renal inner medulla to a pure cell fraction. mRNA was isolated from cultivated cells and sorbitol, AR and SDH activity were determined enzymatically in homogenates. Paper-10121500.
Taken together, the activation of PI3K and p38 MAPK by curcumin augmented the expression of the AR gene via Nrf2, and increased AR activity may be an important cellular response against oxidative stress. Paper-13346956.
The observations are consistent with diffusion of circulating glucose into the lumen, its conversion via AR to sorbitol which accumulates in the lumen and the action of SDH on sorbitol to produce fructose. Paper-11830645.
Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. Paper-13560285.
Many of the complications of diabetes appear to be closely linked to increased conversion of tissue glucose to sorbitol which is catalysed by aldose reductase ( aldehyde reductase 2, ALR2). Paper-6524729.
These results suggest that AR is a cardioprotective protein and that its activation in the ischemic heart is due to peroxynitrite- mediated oxidation of Cys-298 to sulfenic acid via the PI3K/Akt/endothelial NOS pathway. Paper-14301443.
However the actual pattern (amplitude, time course and regional occurrence) of the upregulation of each of the putative (TauT, CDO and CSD) and established ( AR, SMIT and BGT1) osmosensitive genes differs markedly. Paper-8395287.
Human placental aldose reductase ( open reading frame of 316 amino acids) has a 65% identity (identical plus conservative substitutions) to human liver and placental aldehyde reductase ( open reading frame of 325 amino acids). Paper-6145997.
There was a highly significant correlation between increased aldose reductase ( ALR2) expression, CAT, CuZnSOD, and GPX mRNA levels under HG conditions and polymorphisms of ALR2 in the patients with nephropathy ( P < 0.00001). Paper-9877032.
Cellulose acetate zymograms of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (AHD), aldehyde reductase ( AHR), aldehyde oxidase ( AOX) and xanthine oxidase (XOX) extracted from horse tissues were examined. Paper-4544762.
Treatment of HT29 cells with AR inhibitor, sorbinil or zopolrestat, prevented the EGF- and bFGF- induced DNA binding activity of E2F-1 and phosphorylation of retinoblastoma protein. Paper-14773223.
Inhibition of phosphatidylinositol 3-kinase ( PI3K) and p38 mitogen- activated protein kinase ( MAPK) significantly suppressed the curcumin-augmented mRNA levels and promoter activity of the AR gene. Paper-13346956.
Contribution of osmotic stress was assessed by HPLC measurement of sorbitol and by observing the effect of blocking sorbitol accumulation by aldose reductase ( AR) null mutation in the SDH deficient mice. Paper-13059330.
Treatment with antisense AR, which decreased the AR activity by >80%, attenuated PKC activation in TNF-alpha, bFGF, Ang-II, and PDGF-AB-stimulated VSMC and prevented TNF-alpha-induced proliferation. Paper-9169309.
Herein, we report that inhibition of AR prevents epidermal growth factor ( EGF)- and basic fibroblast growth factor (bFGF)-induced HT29 cell proliferation by accumulating cells at G(1) phase of cell cycle. Paper-14773223.
These results suggested that AR may act as a survival factor in these cells and that the EGF receptor-ERK pathway is the major signaling pathway involved in the upregulation of AR expression under oxidative stress. Paper-8860831.
These genes belong to very different biochemical families: csn2 (component of the Cop9 signalosome), aldose reductase (a metabolic enzyme) and brf1 (subunit of the RNA polymerase II complex), S-adenosyl homocysteine hydrolase and Bub1. Paper-14383645.
Very little information is available concerning the expression of the enzymes of sorbitol metabolism ( aldose reductase ( AR) and sorbitol dehydrogenase ( SDH)) on the RNA level under different osmotic conditions. Paper-1756149.
However, in testis, the cells that express these 2 enzymes differed; whereas AR was expressed in Sertoli cells and to lesser extent in spermatogenic cells, SDH was detected in spermatogenic cells of seminiferous tubules. Paper-9295156.
In addition, Hcy might reduce surfactant protein B ( SP-B) expression in the cells, which could be significantly attenuated by Alrestatin, an AR inhibitor, indicating a damaging role of Hcy-induced AR elevation in the lung. Paper-11216905.
ADR is present in continuously proliferating (transformed) lymphoblastoid cell lines and in mitogen- or interleukin 2-stimulated human peripheral blood leukocytes (PBL) but is not detectable in extracts from resting (unstimulated) PBL. Paper-5046034.
The expression of other enzymes involved in BH(4) biosynthesis, including aldose reductase ( AKR1B1), carbonyl reductase ( CBR1 and CBR3), GTP-cyclohydrolase I ( GCH1), and 6-pyruvoyltetrahydrobiopterin ( PTS), was also examined. Paper-13136535.
Tonicity-responsive enhancer binding protein ( TonEBP) regulates transcription of tonicity responsive genes such as the sodium-myo-inositol cotransporter (SMIT), the sodium-chloride-betaine cotransporter (BGT1), and aldose reductase ( AR). Paper-8468801.
The absence of fructose and gluconic acid from cultured lens epithelium suggests that the epithelial cells primarily contain AR, whereas differentiated fiber cells also contain SDH and glucose dehydrogenase. Paper-1655556.
BACKGROUND: In France, the regional pharmacovigilance centres manage drug overdose as adverse drug reactions (ADRs) using the French ADR causality assessment method, and some poison control centres (e.g. in Paris) do likewise for the most serious cases. Paper-11619960.
A strong immunoreactivity to the anti- AR antibody was observed in granulosa cells and epithelia of the oviduct, endometrium, and endometrial glands, and virtually the same tissues were strongly stained with the anti- SDH antibody. Paper-10023584.
The relative abundance of aldehyde reductase ( AR1) and AR2 mRNA was quantitated by filter hybridization of RNA from several human retinal pigment epithelial cell lines exposed to hyperglycemic and hyperosmolar conditions in vitro. Paper-97174.
Induction of IR resulted in increased ischemic injury, reduced ATP levels, increases in L/ P ratio, and poor cardiac function in BBZ rat hearts, while inhibition of AR or SDH attenuated these changes and protected hearts from IR injury. Paper-14338388.
The expression of AKR1B1 in the additional cell lines exhibited significant correlations with sensitivities to 8 of the 23 drugs examined, while that of CTSH displayed a significant negative correlation with only one (MS-247) of the 27 drugs examined. Paper-10197501.
Changes in the relative levels of transcripts of genes coding for aldose reductase ( AR) and sorbitol dehydrogenase ( SoDH) closely matched those of diapause intensity and thus appeared as promising molecular markers of diapause and its development. Paper-12699402.
A number of studies have shown that the polyol pathway, consisting of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH), contributes to ischemia-reperfusion (I/R)-induced myocardial infarction due to depletion of ATP. Paper-15154908.
The quantitative measurements of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) gene expression in various rat tissues were performed by the competitive reverse transcription-polymerase chain reaction ( RT-PCR). Paper-9382390.
Rat hearts were isolated and retrogradely perfused with either Krebs' buffer containing 1 microM AR inhibitor, zopolrestat, or 200 nM SDH inhibitor, CP-170,711, and challenged by 30 min of regional ischemia and 45 min of reperfusion. Paper-15154908.
At the end of the experiment biochemical parameters such as lipid peroxidation, aldose reductase ( AR), sorbitol dehydrogenase ( SDH), reduced glutathione, protein content, and protein carbonyls were measured in the lens. Paper-9703869.
These results suggested that BBR could ameliorate renal dysfunction in DN rats, which may be ascribed to inhibition of AR in mesangium, reduction of oxidative stress, and amelioration of extracellular matrix synthesis and cell proliferation. Paper-12831913.
However, application of aldose reductase ( AR) inhibitor was able to reverse the changes in P-gp levels in the lenses of galactose-fed rats, confirming the role of AR and involvement of the polyol pathway in cataract formation. Paper-12383030.
Many of the compounds which are substrates for AKR1A1 also serve as substrates for AKR1B1, though the latter enzyme was shown to display a specific activity significantly less than that of AKR1A1 for most of the aromatic and aliphatic aldehydes studied. Paper-2039223.
CONCLUSION: The present data show a difference in the association of variations in ALR2, iNOS and TNFB genes with DR, when compared to our previous reports; this could be attributed to differences between the study populations of the past and present report. Paper-15504856.
These results indicate that AR is a potent regulator of TGF-β1 induced expression of FN in human mesangial cells: it suggests that inhibition of this enzyme may be useful to prevented extracellular matrix ( ECM) deposition in glomerulosclerosis. Paper-14555408.
Aldose reductase regulates high glucose- induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. Paper-13560285.
For the biochemical analysis, we measured the enzyme activity of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) and the sorbitol levels using 20, 40 and 60 week old OLETF or control Long-Evans Tokushima Otsuka (LETO) rats. Paper-9055106.
We found that basic fibroblast growth factor ( bFGF), acidic fibroblast growth factor ( aFGF), epidermal growth factor ( EGF), and hypertonic NaCl were able to increase the expression of AR in astrocytes. Paper-1077799.
We propose that, for the biosynthesis of BH(4) in peripheral tissues, SR activity may be substituted by aldose reductase ( AR), carbonyl reductase ( CR), and dihydrofolate reductase, whereas, in the brain, only AR and CR are fully present. Paper-9017302.
Lenticular sorbitol level was significantly increased in the SDH deficient mice, and blocking sorbitol accumulation by the AR null mutation prevented cataract development, demonstrating the contribution of osmotic stress in cataract development. Paper-13059330.
The osmotic response element (ORE) differs from the nuclear factor-kappaB ( NF-kappaB) binding sequence by a single base pair; therefore, we investigated the involvement of NF-kappaB in the induction of aldose reductase ( AR) by curcumin. Paper-12989871.
Aldose reductase ( AR) was proven to be one of the TGF-beta1 responsive genes in cultured rat mesangial cells using the SSH-PCR method and there were positive correlation between the AR and TGF-beta1 in our previous studies. Paper-14155397.
To further understand the involvement of the polyol pathway, the mice with deletion of enzymes in the polyol pathway, AR, and sorbitol dehydrogenase ( SD), which is the second enzyme in this pathway, were challenged with similar cerebral ischemic injury. Paper-13350210.
These data indicate that AR and SDH are key modulators of myocardial IR injury in BBZ rat hearts and that inhibition of polyol pathway could in principle be used as a therapeutic adjunct for protection of ischemic myocardium in Type 2 diabetic patients. Paper-14338388.
Furthermore, our results suggest the binding site residues deviating between ALR1 and ALR2 influence ligand affinity in a complex interplay, presumably involving changes of dynamic properties and differences of the solvation/desolvation balance upon ligand binding. Paper-14451011.
The RT-PCR system developed in this study may be a useful tool in ascertaining the relative contributions of AR and SDH to the metabolic derangements resulting from the acceleration of polyol pathway activity in the target organ of diabetic complications. Paper-8909089.
In particular for the potent inhibitor CMD, the rotameric state of the conserved residue Trp219 (Trp220 in ALR1) is important in forming a pi-stacking interaction with the inhibitor in ALR2 and contributes to the difference in the binding of the inhibitor to the enzymes. Paper-14670645.
Western blotting of extracts from brain, heart, kidney, liver, lung, prostate, skeletal muscle, small intestine, spleen and testis showed that AKR7A2 is present in all of the organs examined, and AKR1B1 is similarly widely distributed in human tissues. Paper-2039223.
RESULTS: Sorbitol concentration in these cells at 300 mosmol/l was 4.4+/-0.3 vs 78+/-3.6 micro mol/g protein at 600 mosmol/l. At steady-state conditions at 300 mosmol/l, AR activity was nearly the same as SDH activity (15.1+/-1.6 vs 16.6+/-2.0 U/g protein). Paper-10121500.
The application of an AR inhibitor, SNK-860, to the high glucose medium ameliorated the increased sorbitol and fructose contents and the reduced AKR1A4 mRNA expression, while it had no effect on mRNA expressions for SAA3, ANGPTL4 or Evi3. Paper-12052622.
Herein we report that inhibition/antisense abolition of polyol pathway enzyme, aldose reductase ( AR) inhibited the TNF-alpha- induced synthesis of prostaglandin E2 and the activity of cyclooxygenase ( Cox) in human colon cancer cells, Caco-2. Paper-13261718.
In addition, 3, 7 and 14 days of water deprivation caused a significant increase in aldose reductase ( AR), myo-inositol (SMIT), betaine/ GABA (BGT-1) and taurine (TauT) transporter mRNA expression, which is indicative of an increase in TonEBP activity. Paper-14356524.
Aldose Reductase Inhibition Prevents Hypoxia- induced Increase in Hypoxia-inducible Factor-1{alpha} (HIF-1{alpha}) and Vascular Endothelial Growth Factor ( VEGF) by Regulating 26 S Proteasome-mediated Protein Degradation in Human Colon Cancer Cells. Paper-16053683.
These findings are the first to show that AR contributes to iron- and transferrin-related oxidative stress associated with cerebral ischemic injury, suggesting that inhibition of AR but not SD may have therapeutic potential against cerebral ischemic injury. Paper-13350210.
The combination of polymorphisms of VEGF together with the aldose reductase ( ALR2) gene showed that in the nephropaths, 8 of the 83 subjects had the VEGF I allele together with the Z+2 5'ALR2 allele compared with 27 of the 62 uncomplicated patients (chi(2)=26.7, P<.00001). Paper-9715409.
The values of Ki and Kies (apparent dissociation constants for inhibitor from enzyme-inhibitor and enzyme-inhibitor-substrate complexes, respectively) for the interactions of ponalrestat with ALR1 and ALR2 has been calculated by non-linear fitting of kinetic data. Paper-6524729.
Conversely, the broad-spectrum MMP inhibitor GM6001 or the EGFR inhibitor AG1478 diminished phosphorylation of EGFR, p38, and ERK1/2, the induction of AR mRNA and protein, and AR promoter reporter activity in response to hypertonicity. Paper-13734398.
Specifically, we investigated, (a) changes in glucose flux via cardiac AR and SDH as a function of diabetes duration, (b) ischemic injury and function after IR, (c) the effect of inhibition of AR or SDH on ischemic injury and function. Paper-14338388.
Concentrations of D-glucose, D-fructose and D-sorbitol were quantified in porcine epididymal fluid by spectrofluorimetric assays and aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) were located immunohistochemically in the epididymal epithelium. Paper-11830645.
We previously found that lack of aldose reductase ( AR), the first enzyme of the polyol pathway, attenuated the increase in transferrin ( Tf) level in I/ R brain, suggesting that AR contributes to iron-catalyzed free radical-induced damage. Paper-12903793.
Severe prematurity (less than 28 weeks) gestation and diseases of prematurity (eg, RDS, apnea, and necrotizing enterocolitis) as well as the use of mechanical ventilation and parenteral nutrition were associated with highly significant increase in ADR occurrence. Paper-4512174.
Inhibition of AR also prevented HG- and TNF-alpha- induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G1/ S transition regulatory proteins such as cyclin D1, cyclin E, cdk-4, c-myc, and proliferative cell nuclear antigen. Paper-15062728.
Our results in mouse hepatocyte AML12 cells show that AR overexpression caused strong suppression of PPARalpha/delta activity (74%, p < 0.001) together with significant down-regulation of mRNA expression for acetyl-CoA oxidase and carnitine palmitoyltransferase-1. Paper-12832354.
Inhibition of AR also prevented EGF- and bFGF- induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G(1)-S transition regulatory proteins such as cyclin D1, cdk4, proliferating cell nuclear antigen, cyclin E, and c-myc. Paper-14773223.
We also eluted high titers of anti- AR and anti- SOD2 IgG(4) from microdissected glomeruli of three biopsies of MN kidneys but not from biopsies of other glomerulonephritides characterized by IgG deposition (five lupus nephritis and two membranoproliferative glomerulonephritis). Paper-14183315.
We previously investigated the correlations between the expression of 9216 genes and various chemosensitivities in a panel of 39 human cancer cell lines(1)) and found that the expression levels of AKR1B1 and CTSH were correlated with sensitivity and resistance to multiple drugs, respectively. Paper-10197501.
To investigate the polyol pathway activity in Schwann cells, we determined the mRNA levels of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) in cultured cells under hyperglycemic or hyperosmotic conditions using competitive RT-PCR technique. Paper-8821113.
The biochemical parameters including aldose reductase enzyme ( AR) activity and lipid peroxidation (MDA), and histopathological changes such as retinal capillary basement membrane thickness (RCBMT) and vascular endothelial growth factor ( VEGF) expression were evaluated. Paper-13283013.
METHODS: The MDR phenotype MCF-7/ ADR cells were treated with recombinant human interferon (IFN)-alpha2b (rhIFN-alpha2b) at different doses for varied length of time, and the expressions of HLA and B7 were determined by flow cytometry (FCM) and compared with those of non-treated cells. Paper-9478536.
Here we examine expression of K(D) channel subunits in Kv1-Kv3 families in immortalized gastric epithelial cells GES and various gastric cancer cells (including AGS, KATOIII, MKN28, MKN45, MGC803, SGC7901, SGC7901/ ADR and SGC7901/VCR), and their roles in cell proliferation. Paper-11508109.
RESULTS: 19F-NMR spectra indicate that incubation of purified dog lenses AR with 3-FG results in the formation of 3-fluoro-3-deoxy-D-sorbitol (3-FS) and that incubation of dog liver sorbitol dehydrogenase ( SDH) with 3-FS results in the formation of 3-fluoro-3-deoxy-D-fructose (3-FF). Paper-1655556.
AKR1B10 is an aldose reductase ( AR) homologue overexpressed in liver cancer and various forms of that enzyme in carcinomas catalyze the reduction of anticancer drugs, potential cytostatic drug, and dl-glyceraldehyde but do not catalyze the reduction of glucose. Paper-14396548.
The study addressed the role for aldose reductase ( AR) in 1) retinal oxidative stress and vascular endothelial growth factor ( VEGF) overexpression in early diabetes, and 2) high glucose-induced oxidative stress in retinal endothelial cells. Paper-9877035.
CONCLUSION: These data suggest that the activation of the polyol pathway by AGEs, more marked in genetic conditions with increased AR activity, may contribute to the pathogenesis of diabetic glomerulopathy, through enhancing mesangial cell expression of TGF-beta1 and type IV collagen. Paper-10903414.
Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme ( TACE) ( ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. Paper-13560285.
RESULTS: In the EIU rat eye AqH, both the number of infiltrating cells and protein concentrations of the inflammatory markers, TNF-alpha, NO, and PGE(2) were significantly higher than in the control rats, and inhibition of AR by zopolrestat suppressed the LPS-induced increases. Paper-12485930.
We found evidence that metalloproteinase (MMP)-dependent activation of the epidermal growth factor receptor ( EGFR) signals to TonEBP and stimulates the expression of the TonEBP target gene aldose reductase ( AR) under hypertonic conditions. Paper-13734398.
Collectively, these data indicate that fructose is produced by coordinately expressed AR and SDH in the egg and epithelia of the oviduct and suggest that the resulting sorbitol and fructose can be used as energy sources for spermatozoa motility during the fertilization process. Paper-10023584.
0. After validating the five-level intact ( INT) model with previous in vitro studies, the L3/L4 level of the INT model was modified to either insert an artificial disc (ProDisc II; ADR) or incorporate bilateral posterior lumbar interbody fusion (PLIF) cages with a pedicle screw fixation system. Paper-13536086.
Moreover, when the 12 cell lines were divided into high-expressing and low-expressing groups, a comparison of these groups using Mann-Whitney's U test revealed that high expression levels of AKR1B1 and CTSH were related to sensitivity to 21 of the drugs and resistance to 8 of the drugs, respectively. Paper-10197501.
RESULTS: At the doses smaller than 1x10(3) IU/ml, rhIFN-alpha2b did not exhibit significant inhibition on MCF-7/ ADR cell growth, but HLA and B7 expressions were enhanced in a dose- and time-dependent fashion and significant up-regulation occurred 24 h after 400 IU/ml rhIFN-alpha2b treatment. Paper-9478536.
Complementary DNA clones encoding human aflatoxin B(1) aldehyde reductase ( AKR7A2), aldehyde reductase ( AKR1A1), aldose reductase ( AKR1B1), dihydrodiol dehydrogenase 1 ( AKR1C1) and chlordecone reductase (AKR1C4) have been expressed in Escherichia coli. Paper-2039223.
We found that inhibition of AR or sorbitol dehydrogenase ( SDH), the second enzyme of the polyol pathway, both attenuated the I/ R-mediated increases in HIF-1alpha, Tf, TfR, and intracellular iron content and reduced the I/ R-induced infarct area of the heart. Paper-12903793.
Herein we show that inhibition of the aldehyde-metabolizing enzyme aldose reductase ( AR) inhibits NF-kappa B activation during restenosis of balloon-injured rat carotid arteries as well as VSMC proliferation due to tumor necrosis factor alpha ( TNF-alpha) stimulation. Paper-9169309.
Blood glucose, microalbuminuria, kidney index, total antioxidative capacity, laminin, advanced glycation end products (AGE), aldose reductase ( AR) activity, and the relative quantity of transforming growth factor beta1 (TGF- beta1) mRNA were measured by different methods. Paper-11111826.
We have also sequenced a selected material of 37 sporadic cases of more severe hypospadias for mutations in the androgen receptor AR, SRD5A2, and 17beta-hydroxysteroid dehydrogenase HSD17B3 genes and found only two previously described mutations, one in the AR and one in the SRD5A2 gene. Paper-11513019.
Collectively, these observations suggest that AR is an obligatory mediator of growth factor- induced up-regulation of COX-2, PGE(2), and growth of Caco-2 cells, indicating that inhibition of AR may be a novel therapeutic approach in preventing the progression of colon cancer. Paper-12254317.
The structure clarified that fidarestat was located in the active site by hydrophilic and hydrophobic interactions and that the carbamoyl group of fidarestat was a very effective substituent for affinity to AR and for selectivity between AR and aldehyde reductase ( AHR). Paper-8394788.
Inhibition of AR prevented growth factor- induced COX-2 activity, protein, and mRNA and significantly decreased activation of nuclear factor-kappaB and protein kinase C (PKC) and phosphorylation of PKC-beta2 as well as progression of Caco-2 cell growth but had no effect on COX-1 activity. Paper-12254317.
Under identical conditions, treatment with AR inhibitors also prevented the activation of protein kinase C (PKC) by TNF-alpha, bFGF, Ang-II, and PDGF-AB but not phorbol esters, indicating that AR inhibitors prevent PKC stimulation or the availability of its activator but not PKC itself. Paper-9169309.
The expression of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH), which, in concert, catalyze the conversion of glucose to fructose via sorbitol, in the rat ovary, oviduct, and uterus, was investigated by immunohistochemical and biochemical analyses. Paper-10023584.
Interestingly, there was a remarkable difference between the two sublines MCF-7 and MCF-7/ ADR: Both the tissue and serum levels of CD44 isoforms indicated that the development of multidrug resistance is accompanied by an alteration in the expression of membrane proteins discussed to be involved in metastasis. Paper-1271841.
Mouse glomeruli and primary cultures of MCs from hAR TG and wild-type (WT) mice were studied regarding the changes in AR activity, transforming growth factor-beta1 ( TGF-beta1) and type IV collagen mRNA and protein levels, in response to BSA modified by advanced glycation end-products (AGE-BSA). Paper-10903414.
Our results indicate that inhibition of AR prevents RWE -induced apoptotic cell death as measured by annexin-v staining, increase in the activation of NF-kappaB and expression of inflammatory markers such as inducible nitric oxide synthase ( iNOS), cycloxygenase (COX)-2, Prostaglandin ( PG) E(2), IL-6 and IL-8. Paper-13917517.
Together, at both the mRNA and protein levels, SAHA suppressed the expression of reticulocalbin 1 precursor (RCN1), annexin A3 ( ANXA3) and heat shock 27 kDa protein 1 (HSP27), while increasing the expression of aldose reductase ( AR), triosephosphate isomerase 1 ( TPI) and manganese superoxide dismutase (SOD2). Paper-14347527.
Nonradioactive in situ hybridization studies on sections from formalin-fixed and paraffin-embedded, normally concentrating kidneys showed strong expression of BGT, SMIT, and AR mRNAs in interstitial and collecting duct cells of the papilla, whereas expression of SDH mRNA was much weaker in both cell types. Paper-1897519.
We investigated the relationship between diabetic retinopathy (DR) and three polymorphisms, C(-106)T in the aldose reductase ( ALR2) gene, 4G/5G in the plasminogen activator inhibitor-1 ( PAI-1) gene and C677T in the methylenetetrahydrofolate reductase ( MTHFR) gene, in 210 Euro-Brazilian type 2 diabetic patients. Paper-9961816.
Inhibition of AR attenuated TNF-alpha and hyperglycemia-induced activation of protein kinase C (PKC), phosphorylation of the inhibitory subunit of nuclear factor-kappaB ( NF-kappaB), and stimulation of NF-kappaB, but it did not prevent the activation of NF-kappaB and PKC by phorbol ester. Paper-9707014.
The silencing lasted only 3 d after introduction of the TonEBP-siRNA's. As expected, TonEBP-driven reporter gene expression and expression of the sodium/myo-inositol cotransproter (SMIT), aldose reductase ( AR) and heat shock protein 70 (HSP70) mRNA were significantly decreased in cells where TonEBP expression was silenced. Paper-9767071.
The polyol pathway consists of two enzymes aldose reductase ( AR) and sorbitol dehydrogenase ( SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor. Paper-9905376.
Herein we report that inhibition of the polyol pathway enzyme aldose reductase ( AR) by two structurally unrelated inhibitors--sorbinil and tolrestat--prevents, in the human lens epithelial cell line B-3, the apoptosis and activation of caspase-3 caused by exposure to high glucose levels or TNF-alpha. Paper-9707014.
Here we report that TGF-β1-induced expression of fibronectin ( FN) depends on the activity of aldose reductase ( AR) in human mesangial cells (HMCs).The results show that TGF-β1 increased the expression of FN, which attenuated by pharmacological inhibition of AR or knockdown of the enzyme by small interfering RNA (siRNA). Paper-14555408.
Two major forms of aldehyde reductase ( AHR) activity were resolved following zone electrophoresis of mouse lung homogenates and distinguished by their differential substrate and inhibitor specificities: alcohol dehydrogenase ( ADH) C2 and carbonyl reductase ( CBR). Paper-5514514.
The enzymatic activities of glutathione s-transferase ( GST), NAD(P)H:quinone oxidoreductase (QR), aldehyde reductase ( AR), and glutathione reductase ( GR) were measured by kinetics methods using UV-Vis spectroscopy, and analyzed statistically by Student's t-test. Paper-9838853.
To explore the relationships between polyol pathway-related enzymes and pathologic features, we examined the immunohistochemical expression of aldose reductase ( AR) and sorbitol dehydrogenase ( SDH) in the peripheral nerve and kidney tissues collected postmortem from diabetic patients and compared it with those from non-diabetic patients. Paper-9041323.
The sequential expression of NKCC2, TonEBP, and its targets AR and UT-A and the reduced expression TonEBP and its targets in response to furosemide treatment support the hypothesis that local hypertonicity produced by the activity of NKCC2 activates TonEBP during development. Paper-12396457.
The various cell types (epithelial, endothelial and interstitial cells) differed in their expression pattern and intensity of AR, SDH, BGT and SMIT mRNA, but the inner medullary cells responded uniformly to a decrease in extracellular tonicity with a reduction, and to an increase with enhancement of their AR, BGT and SMIT expression. Paper-1739702.
Following acute salt-loading, mRNA levels of TauT, CDO, CSD, SMIT, BGT1 and AR were increased in cerebral cortex while SMIT- and BGT1-mRNA levels only were increased in striatum and habenula.TauT, CDO and CSD genes may be upregulated in brain of salt-loaded rats but the upregulation of the TauT gene appears more widespread. Paper-8395287.
METHODS: In this study, we examined the effect of the HMG-CoA-reductase inhibitor atorvastatin on the expression of aldose reductase ( AR, AKR1B1), aldehyde reductase (AldR, AKR1A1) and small intestine reductase (SIR, AKR1B10) in human umbilical vein endothelial cells (HUVEC) and human proximal tubular epithelial cells (PTEC) by RT-PCR. Paper-13813497.
Specific antibodies raised against AKR7A2, AKR1A1, AKR1B1, AKR1C1 and AKR1C4 have been used to show the presence of all of the reductases in human hepatic cytosol; the levels of AKR1B1 and AKR1C1 were markedly elevated in livers with alcohol-associated injury, and indeed AKR1B1 was only detectable in livers with evidence of alcoholic liver disease. Paper-2039223.
Collectively, these results show that AR mediates EGF- and bFGF- induced colon cancer cell proliferation by activating or expressing G(1)-S phase proteins such as E2F-1, cdks, and cyclins through the reactive oxygen species/phosphoinositide 3-kinase/ AKT pathway, indicating the use of AR inhibitors in the prevention of colon carcinogenesis. Paper-14773223.
These synonyms are used for gene AKR1B1 (aldo-keto reductase family 1, member B1 (aldose reductase)): MGC1804, AR, ALR2, ALDR1, Aldose reductase, Aldo-keto reductase family 1 member B1, Aldehyde reductase, ADR.
These accession numbers are used for gene AKR1B1: Q6ICP2 (UNIPROT__AC), Q6FGA4 (UNIPROT__AC), CR592404 (NCBI_GENBANK__AC), BC010391 (NCBI_GENBANK__AC).
AKR1B1 is a homologue of Y39G8B.1 (hypothetical protein) from Caenorhabditis elegans.
AKR1B1 is a homologue of Os05g0456300 (Os05g0456300) from Oryza sativa Japonica Group.
AKR1B1 is a homologue of Os01g0847700 (Os01g0847700) from Oryza sativa Japonica Group.
AKR1B1 is a homologue of Os01g0847600 (Os01g0847600) from Oryza sativa Japonica Group.
AKR1B1 is a homologue of NCU08384 (xylose reductase) from Neurospora crassa OR74A.
AKR1B1 is a homologue of MGG_03648 (hypothetical protein) from Magnaporthe oryzae 70-15.
AKR1B1 is a homologue of LOC607537 (similar to Aldose reductase (AR) (Aldehyde reductase)) from Canis lupus familiaris.
AKR1B1 is a homologue of LOC482334 (similar to Aldose reductase (AR) (Aldehyde reductase)) from Canis lupus familiaris.
AKR1B1 is a homologue of LOC425137 (similar to aldose reductase) from Gallus gallus.
AKR1B1 is a homologue of LOC418170 (similar to aldose reductase) from Gallus gallus.
AKR1B1 is a homologue of KLLA0E21627g (hypothetical protein) from Kluyveromyces lactis NRRL Y-1140.
AKR1B1 is a homologue of GRE3 (Gre3p) from Saccharomyces cerevisiae S288c.
AKR1B1 is a homologue of CG6084 (CG6084 gene product from transcript CG6084-RB) from Drosophila melanogaster.
AKR1B1 is a homologue of AT3G53880 (aldo/keto reductase family protein) from Arabidopsis thaliana.
AKR1B1 is a homologue of AT2G37790 (aldo/keto reductase family protein) from Arabidopsis thaliana.
AKR1B1 is a homologue of AT2G37770 (aldo/keto reductase family protein) from Arabidopsis thaliana.
AKR1B1 is a homologue of Akr1b3 (aldo-keto reductase family 1, member B3 (aldose reductase)) from Mus musculus.
AKR1B1 is a homologue of AKR1B10 (aldo-keto reductase family 1, member B10 (aldose reductase)) from Gallus gallus.
AKR1B1 is a homologue of AKR1B1 (aldo-keto reductase family 1, member B1 (aldose reductase)) from Pan troglodytes.
AKR1B1 is a homologue of AKR1B1 (aldo-keto reductase family 1, member B1 (aldose reductase)) from Bos taurus.
AKR1B1 is a homologue of AKR1B1 (aldo-keto reductase family 1, member B1 (aldose reductase)) from Gallus gallus.
AKR1B1 is a homologue of Akr1b1 (aldo-keto reductase family 1, member B1 (aldose reductase)) from Rattus norvegicus.
AKR1B1 is a homologue of akr1b1 (aldo-keto reductase family 1, member B1 (aldose reductase)) from Danio rerio.
AKR1B1 is a homologue of AGOS_ACL107C (ACL107Cp) from Ashbya gossypii ATCC 10895.
AKR1B1 is a homologue of AgaP_AGAP011050 (AGAP011050-PA) from Anopheles gambiae str. PEST.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.