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Double staining demonstrated that elafin was co-localized with tTG. Paper-9349656.
In light of these findings, we thus focused on the status of elafin in CF lung. Paper-14337348.
Because of this cross reactivity, it was not possible to differentiate between MPI and ESI. Paper-1062951.
Automated sub-ppm mass accuracy on an ESI- TOF for use with drug discovery compound libraries. Paper-13409181.
Human alveolar macrophages express elafin and secretory leukocyte protease inhibitor. Paper-8962977.
The polyclonal antibodies usually used to detect MPI did not distinguish between MPI and ESI. Paper-1062951.
Furthermore, elafin and SLPI are "defensin-like" molecules with broad antimicrobial activity. Paper-12475860.
Elafin stained predominantly in the epithelium and SLPI in mucosal inflammatory cells. Paper-12475860.
CONCLUSIONS: the expression of tTG and elafin increased in atherosclerotic coronary arteries. Paper-9349656.
We showed in the present study that elafin is cleaved in sputum from individuals with CF. Paper-14337348.
We propose the acronym SKALP (skin-derived antileucoprotease) as a name for these new proteinase inhibitors. Paper-6503869.
During culture, skin-derived antileukoproteinase and keratin 17 were expressed only in the epithelial tongue. Paper-12884037.
In contrast, three days after ICU admission, there was a significant drop of HNE/ PI3 ratio in the at-risk controls. Paper-13605087.
In particular, CHI3L1 and PI3/ elafin may be useful as new prognostic markers and new therapeutic targets. Paper-14298315.
Elafin and SLPI may be added to the list of defensin-like peptides with diminished induction in CD versus UC. Paper-12475860.
Expression of tissue transglutaminase and elafin in human coronary artery: implication for plaque instability. Paper-9349656.
Purification and characterization of elastase-specific inhibitor. Sequence homology with mucus proteinase inhibitor. Paper-7085091.
Our findings indicate that elafin and SLPI may be gene therapy targets for the treatment of atheroma. Paper-10321234.
NE plays a pivotal role in the process as only NE inhibitors are able to inhibit elafin degradation. Paper-14337348.
Oxidized elafin and trappin poorly inhibit the elastolytic activity of neutrophil elastase and proteinase 3. Paper-11217713.
Electrophoretic analysis confirmed digestion of alpha1PI by MMP-8 but no digestion of either SLPI or elafin was observed. Paper-9388404.
The properties of the urinary anti-elastase activity in psoriatic patients were indistinguishable from that of epidermal SKALP. Paper-7528366.
Plasma neutrophil elastase and elafin imbalance is associated with acute respiratory distress syndrome (ARDS) development. Paper-13605087.
Cox regression analysis further confirmed that PI3 and CHI3L1 levels are survival markers independent from patient age and sex. Paper-14298315.
Levels of mRNA and immunostaining of the antiproteases elafin and SLPI were enhanced strongly in inflamed versus noninflamed UC. Paper-12475860.
The aim of this study was to determine if SLPI and elafin are similarly susceptible to degradation by this neutrophil-specific MMP. Paper-9388404.
Persistent ESI/TI in Swan neck catheters can be successfully treated with surgical exposure and removal of the subcutaneous external cuff. Paper-834069.
Importantly, high levels of CHI3L1 (p = 0.036) and PI3/ elafin mRNA (p = 0.0004) were significantly correlated with poor survival. Paper-14298315.
A considerable fraction of beta-globin undergoes incomplete desolvation during ESI, thereby reducing the intensity of bare [beta + zH](z+) ions. Paper-13321908.
The five mucosal transcripts aldolase B, elafin, MST-1, simNIPhom and SLC6A14 were analyzed using quantitative real-time PCR. Paper-12987980.
Before the onset (7-days period prior to ARDS diagnosis), we only observed significantly elevated HNE, but the HNE- PI3 balance remained normal. Paper-13605087.
Further in vitro studies demonstrated that incubation of recombinant elafin with excess of NE leads to the rapid cleavage of the inhibitor. Paper-14337348.
CONCLUSIONS/SIGNIFICANCE: Plasma profiles of PI3, HNE, and HNE/ PI3 may be useful clinical biomarkers in monitoring the development of ARDS. Paper-13605087.
Accumulation of elafin in actinic elastosis of sun-damaged skin: elafin binds to elastin and prevents elastolytic degradation. Paper-13240241.
Oxidized elafin and trappin have, however, reasonable affinities for NE (K(i) = 4.0-9.2 x 10(-9) M) and for Pr3 (K(i) = 2.5-5.0 x 10(-8) M). Paper-11217713.
Crystal structure of an elastase-specific inhibitor elafin complexed with porcine pancreatic elastase determined at 1.9 A resolution. Paper-675874.
It is surprising that comparing inflamed versus noninflamed CD, this increase was significantly less pronounced for elafin and even lacking for SLPI. Paper-12475860.
At their physiological concentration, fully oxidized elafin and trappin do not inhibit more than 30% of an equimolar concentration of NE or Pr3. Paper-11217713.
When LPS was given systemically, the mice expressing elafin had reduced levels of serum TNF-alpha compared to the levels in wild-type mice. Paper-9659963.
Elafin prevents lipopolysaccharide- induced AP-1 and NF-kappaB activation via an effect on the ubiquitin-proteasome pathway. Paper-12311240.
An automated, routine method to obtain sub-ppm accurate mass data on a benchtop electrospray ionization time-of-flight ( ESI- TOF) mass spectrometer is described. Paper-13409181.
Elafin and secretory leukocyte protease inhibitor ( SLPI) are two structurally related serine protease inhibitors present in the lung. Paper-8962977.
BACKGROUND: Secretory leukocyte protease inhibitor ( SLPI) and elafin are anti-protease and anti-microbial molecules with a role in innate immune defence. Paper-13628962.
Elafin, an elastase-specific inhibitor, is cleaved by its cognate enzyme neutrophil elastase in sputum from individuals with cystic fibrosis. Paper-14337348.
CONCLUSION: These data suggest that SLPI and elafin have a role in the innate immune defence of the Fallopian tube in infection and ectopic pregnancy. Paper-13628962.
SLPI and elafin were immunolocalised to the Fallopian tube epithelium in biopsies from non-pregnant women and those with ectopic pregnancy. Paper-13628962.
In the present study, we showed by RT-PCR that human alveolar macrophages, but not peripheral blood monocytes, express elafin and SLPI transcripts. Paper-8962977.
Since tissue transglutaminase ( tTG) and elafin act as stabilizing factors, they might play a crucial role in the pathogenesis of acute coronary syndrome. Paper-9349656.
Expression of secretory leukocyte protease inhibitor and elafin in human fallopian tube and in an in-vitro model of Chlamydia trachomatis infection. Paper-13628962.
The structural homology between r- elafin and the C-terminal domain of SLPI confirms the former as a second member of the chelonianin family of proteinase inhibitors. Paper-1030556.
Multifaceted roles of human elafin and secretory leukocyte proteinase inhibitor ( SLPI), two serine protease inhibitors of the chelonianin family. Paper-12720605.
This leads to suppression of beta-globin signals under conditions where the protein ion yield is limited by the charge concentration on the initially formed ESI droplets. Paper-13321908.
Attenuated induction of epithelial and leukocyte serine antiproteases elafin and secretory leukocyte protease inhibitor in Crohn's disease. Paper-12475860.
Examples include high profile protein kinase targets and structurally related PI3 kinases, histone deacetylases, poly(ADP-ribose)polymerase and the molecular chaperone HSP90. Paper-13738145.
Elafin and SLPI are structurally related in that both have a fold with a four-disulfide core or whey acidic protein (WAP) domain responsible for inhibiting proteases. Paper-12720605.
Elafin prevented lipopolysaccharide- induced phosphorylation of AP-1, c-Jun, and JNK but had no effect on phosphorylation of p38. Paper-12311240.
In addition, we show that interleukin-1 beta and tumor necrosis factor induce significant SLPI expression and are major inducers of elafin/pre- elafin expression. Paper-140576.
The partial N-terminal amino-acid sequence of ESI shows some homology with MPI, especially around the reactive site of MPI for human neutrophil elastase. Paper-7085091.
METHODOLOGY/PRINCIPAL FINDINGS: PI3, SLPI, and HNE were measured in plasma samples collected from 148 ARDS patients and 63 critical ill patients at risk for ARDS (controls). Paper-13605087.
These data prompted us to examine the biological consequences of elafin binding to LPS, using tumor necrosis factor (TNF)-alpha release by murine macrophages. Paper-11210263.
High-throughput peptide mass mapping using a microdevice containing trypsin immobilized on a porous polymer monolith coupled to MALDI TOF and ESI TOF mass spectrometers. Paper-9625913.
However, NE in excess was shown to strongly diminish the ability of elafin to bind lipopolysaccharide ( LPS) and its capacity to be immobilized by transglutamination. Paper-14337348.
1. Among them are genes of the known or postulated protease inhibitors elafin, secretory leucocyte protease inhibitor, human epididymis gene product 4, eppin, and huWAP2. Paper-9240115.
Histological inflammation was scored, and HNE, elafin, and SLPI were localized and semiquantified by immunostaining in 51 colonic paraffin sections (23 CD, 11 UC, 17 controls). Paper-12475860.
PI3 and secretory leukocyte proteinase inhibitor ( SLPI) are important low-molecular-weight proteinase inhibitors produced locally at neutrophil infiltration site in the lung. Paper-13605087.
MLP was the least efficient promoter Intermediate between MCMV and MLP was HCMV which was able to induce significant amounts of elafin, particularly in human A549 cells. Paper-1450374.
Under physiological conditions human bronchial mucus contains an elastase-specific inhibitor which is quite different from hitherto known inhibitors: alpha 1-antitrypsin, HI-30, and BSI-TE. Paper-4489101.
Specific recognition of human telomeric G-quadruplex DNA with small molecules and the conformational analysis by ESI mass spectrometry and circular dichroism spectropolarimetry. Paper-13259390.
SLPI and elafin/ trappin-2 are attractive candidates as therapeutic molecules for inhibiting neutrophil serine proteases in inflammatory lung diseases. Paper-12720605.
These results suggest that inhibition by elafin of lipopolysaccharide- induced AP-1 and NF-kappaB activation occurs via an effect on the ubiquitin-proteasome pathway. Paper-12311240.
CHI3L2, IL1B, PI3/ elafin and CHI3L1, which encodes for YKL-40, a putative prognosticator for various diseases, including cancer, were strongly up-regulated in avascular glioma. Paper-14298315.
Moreover, the phosphoinositide 3-OH ( PI3) kinase pathway was required for the maintenance of EFC, as inhibition of PI3 kinase reverted fibroblastoid cells to an epithelial-like phenotype. Paper-9397544.
Regulation of secretory leukocyte proteinase inhibitor ( SLPI) and elastase-specific inhibitor ( ESI/ elafin) in human airway epithelial cells by cytokines and neutrophilic enzymes. Paper-140576.
When radiolabeled insoluble elastin was incubated with recombinant full-length elafin and tissue transglutaminase, insoluble elastin became more resistant to neutrophil elastase digestion. Paper-13240241.
Human alveolar epithelial cells (A549), as well as rat and human primary pulmonary fibroblasts were infected with Ad5-HCMV- EL, Ad5- MLP- EL, Ad5-MCMV- EL and with the control Ad5-dl70/3. Paper-1450374.
Although the controls had elevated plasma PI3 and HNE, their HNE/ PI3 ratio (mean = 6.5; 95% CI, 4.9-8.8) was not significantly different from the healthy individuals (mean = 3.9; 95% CI, 2.7-5.9). Paper-13605087.
Elafin and murine SLPI also reduced endothelial IL-8 release in response to oxidized low density lipoprotein, LPS, and TNF-alpha and macrophage TNF-alpha production in response to LPS. Paper-10321234.
Three promoters were chosen to drive the synthesis of elafin: the small (380 bp) human cytomegalovirus promoter (HCMV), the Ad2 major late promoter ( MLP) and the mouse cytomegalovirus (MCMV) promoter. Paper-1450374.
Analysis with reverse transcriptase-polymerase chain reaction ( RT-PCR) of cells from lavages and of nucleated cells isolated from the peripheral blood showed the production of ESI only, but not of MPI. Paper-1062951.
These results demonstrate that SLPI and elafin are resistant to proteolytic inactivation by MMP-8, a property that may enhance their therapeutic application in neutrophil-mediated inflammatory lung disease. Paper-9388404.
It appears that iTRAQ analyses performed on an ESI QTOF without any special modifications to instrumental parameters produce essentially the same protein ratios as those obtained on a MALDI TOF/ TOF. Paper-13023077.
The effect of MMP-8 on SLPI and elafin was assessed by determining the neutrophil elastase inhibitory capacity (NEIC) and electrophoretic protein profile of both inhibitors following exposure to purified MMP-8. Paper-9388404.
We used two-way analysis of variance ( ANOVA) to compare the iTRAQ ratios that were generated on an ESI QTOF and a matrix-assisted laser desorption/ionization tandem time-of-flight ( MALDI TOF/ TOF). Paper-13023077.
Real-time PCR was performed to quantitate colonic, proinflammatory cytokine IL-8, protease (HNE), and antiprotease mRNA ( elafin and SLPI) in a total of 340 biopsies from 117 patients (47 CD, 45 UC, 25 controls). Paper-12475860.
These data show that regenerating V2Rs respond to urine and the urinary peptides by activation of the Ras-ERK and PI3- Akt pathways, which appear to be important for vomeronasal neural survival and proliferation. Paper-12415825.
In conclusion, this study provides evidence that elafin is cleaved by its cognate enzyme NE present at excessive concentration in CF sputum and that P. aeruginosa infection promotes this effect. Paper-14337348.
Adenoviral gene delivery of elafin and secretory leukocyte protease inhibitor attenuates NF-kappa B-dependent inflammatory responses of human endothelial cells and macrophages to atherogenic stimuli. Paper-10321234.
Incubation of synthetic transglutaminase substrate domain of elafin and elastin molecules in the presence of tissue transglutaminase in vitro resulted in the formation of a higher molecular complex on SDS-PAGE. Paper-13240241.
Elafin and its precursor trappin-2 still inhibit neutrophil serine proteinases when they are covalently bound to extracellular matrix proteins by tissue transglutaminase. Paper-11118660.
Functionally active acid-resistant inhibitors with molecular masses characteristic of the mucus proteinase inhibitor ( MPI, 14 kDa) and elastase-specific inhibitor ( ESI, 7 kDa) were demonstrated by gel chromatography. Paper-1062951.
We demonstrate that the lipid A core-binding proteins polymyxin B ( PB) and LPS- binding protein (LBP) compete with elafin for binding, and that LBP is able to displace prebound elafin from LPS. Paper-11210263.
In the present study, we show that NCI-H322 cells produced higher amounts of both inhibitors than A549 cells and that basal production of SLPI in both cell lines is higher than the production of elafin/pre- elafin. Paper-140576.
BACKGROUND: We conducted an exploratory study of genome-wide gene expression in whole blood and found that the expression of neutrophil elastase inhibitor ( PI3, elafin) was down-regulated during the early phase of ARDS. Paper-13605087.
After hexane/ acetonitrile partitioning lipid-rich samples such as cereals, the extract was cleaned up on a PSA column or tandem graphitized carbon/ PSA column, and determined by ESI- SIM mode LC-MS. Paper-13768622.
In this report we have shown that elafin inhibits the lipopolysaccharide- induced production of monocyte chemoattractant protein-1 in monocytes by inhibiting AP-1 and NF-kappaB activation. Paper-12311240.
With the progress from prior to the onset of ARDS, the plasma level of PI3 declined, whereas HNE was maintained at a higher level, tilting the balance toward more HNE in the circulation as characterized by an increased HNE/ PI3 ratio. Paper-13605087.
METHODS AND RESULTS: immunohistochemical studies on autopsy samples of human coronary arteries revealed the expression of tTG and elafin in the endothelium, medial SMCs, and the ECM in non-atherosclerotic coronary arteries. Paper-9349656.
The naturally occurring neutrophil elastase inhibitors, alpha1-proteinase inhibitor (alpha1PI), secretory leukocyte proteinase inhibitor ( SLPI), and elafin, are potential therapeutic agents in the treatment of neutrophil-mediated lung disease. Paper-9388404.
We recently reported the presence of SLPI and of an elastase-specific inhibitor ( ESI), also called elafin, in the supernatants of two cell lines, NCI-H322 and A549, which have features of Clara cells and type II alveolar cells, respectively. Paper-140576.
Elafin, but not SLPI, mRNA expression was increased time dependently in alveolar macrophages stimulated with Saccharopolyspora rectivirgula antigen (50 microg/ml), a causative agent of hypersensitivity pneumonitis, but not LPS (10 microg/ml). Paper-8962977.
Compared with the controls, the ARDS patients had higher HNE, but lower PI3, at the onset of ARDS, resulting in increased HNE/ PI3 ratio (mean = 14.5; 95% CI, 10.9-19.4, P<0.0001), whereas plasma SLPI was not associated with the risk of ARDS development. Paper-13605087.
Compared to the control group, the TNF, P.aeruginosa and E. coli groups showed increased elafin mRNA and protein in cells (p < 0.05), and contents in the TNF and P.aeruginosa group were higher than in the E. coli group (p< 0.05). Paper-14119254.
Pseudomonas aeruginosa-positive CF sputum, which was found to contain lower elafin levels and higher neutrophil elastase ( NE) activity compared with P. aeruginosa-negative samples, was particularly effective in cleaving recombinant elafin. Paper-14337348.
This review focuses on recent findings revealing that SLPI and elafin/ trappin-2 have many biological functions as diverse as anti-bacterial, anti-fungal, anti-viral, anti-inflammatory and immuno-modulatory functions, in addition to their well-recognized role as protease inhibitors. Paper-12720605.
METHODS: A549 epithelial cells transfected with pEGFP-N1- elafin or pEGFP-N1 were stimulated with tumor necrosis factor ( TNF), P.aeruginosa supernatant and Escherichia coli supernatant followed by co-incubation for 24 h to form P.aeruginosa biofilms. Paper-14119254.
Quantitative real-time PCR analysis showed that SLPI and elafin were constitutively expressed in the Fallopian tube during the menstrual cycle but were increased in ectopic pregnancy (P < 0.05 versus early-mid luteal phase, P < 0.01 versus all phases, respectively). Paper-13628962.
Elafin (or skin-derived antileukoprotease) and secretory leukocyte protease inhibitor ( SLPI) are serine antiproteases antagonizing human neutrophil elastase (HNE), thereby preventing tissue injury from excessive release of proteolytic enzymes by inflammatory cells. Paper-12475860.
Elafin and SLPI are low-molecular weight proteins that were first identified as protease inhibitors in mucous fluids including lung secretions, where they help control excessive proteolysis due to neutrophil serine proteases (elastase, proteinase 3 and cathepsin G). Paper-12720605.
Elastase-specific inhibitor ( ESI) was purified from sputum of patients with chronic bronchitis and compared with mucus proteinase inhibitor ( MPI, BrI) isolated, without the use of affinity chromatography on an enzyme, from non-purulent sputum of a patient with bronchial carcinoma. Paper-7085091.
When LPS was delivered to the lungs, we found that mice expressing elafin had lower serum-to-bronchoalveolar lavage ratios of proinflammatory cytokines, including tumor necrosis factor alpha ( TNF-alpha), macrophage inflammatory protein 2, and monocyte chemoattractant protein 1, than wild-type mice. Paper-9659963.
These results indicate that (1) dermal fibroblasts potentially express elafin on UV irradiation, (2) UV-mediated elafin interacts with elastin, and (3) the elafin- elastin complex protects elastic fibers from elastolytic degradation, leading to the accumulation of elastic fibers in the actinic elastosis of sun-damaged skin. Paper-13240241.
Subsequent amino acid sequencing revealed many peptides involving involucrin cross-linked either to itself or to a variety of other known CE protein components, including cystatin alpha, desmoplakin, elafin, keratins, members of the small proline-rich superfamily, loricrin, and unknown proteins related to the desmoplakin family. Paper-857450.
To counteract the activity of HNE, we have examined the effects of adenoviral gene delivery of the anti-elastases elafin, previously demonstrated within human atheroma, and murine secretory leukocyte protease inhibitor ( SLPI), a related molecule, on the inflammatory responses of human endothelial cells and macrophages to atherogenic stimuli. Paper-10321234.
These synonyms are used for gene PI3 (peptidase inhibitor 3, skin-derived): WFDC14, WAP four-disulfide core domain protein 14, WAP3, Skin-derived antileukoproteinase, SKALP, Protease inhibitor WAP3, PI-3, Peptidase inhibitor 3, MGC13613, ESI, Elastase-specific inhibitor, ELAFIN, Elafin, cementoin.
These accession numbers are used for gene PI3: Q6FG74 (UNIPROT__AC), E1P618 (UNIPROT__AC), BC010952 (NCBI_GENBANK__AC), AA583773 (NCBI_GENBANK__AC).
PI3 is a homologue of PI3 (peptidase inhibitor 3, skin-derived) from Pan troglodytes.
PI3 is a homologue of PI3 (peptidase inhibitor 3, skin-derived) from Canis lupus familiaris.
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