ArticleThe American journal of pathology2007
Protease-activated receptor-2 augments experimental crescentic glomerulonephritis.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- The Many Faces of Protease-Activated Receptor 2 in Kidney Injury.Biomedicines · 2025Review
- Crescents in primary glomerulonephritis: a pattern of injury with dissimilar actors. A pathophysiologic perspective.Pediatric nephrology (Berlin, Germany) · 2022Review
- Factor Xa inhibitor, edoxaban ameliorates renal injury after subtotal nephrectomy by reducing epithelial-mesenchymal transition and inflammatory response.Physiological reports · 2022Article
- PAR2-Induced Tissue Factor Synthesis by Primary Cultures of Human Kidney Tubular Epithelial Cells Is Modified by Glucose Availability.International journal of molecular sciences · 2021Article
- PAR2 Activation on Human Kidney Tubular Epithelial Cells Induces Tissue Factor Synthesis, That Enhances Blood Clotting.Frontiers in physiology · 2021Article
- Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury.Scientific reports · 2019Article
- Endothelium structure and function in kidney health and disease.Nature reviews. Nephrology · 2019Review
- The Kallikrein-Kinin System: A Novel Mediator of IL-17-Driven Anti-Candida Immunity in the Kidney.PLoS pathogens · 2016Article
- Cathepsin S-Dependent Protease-Activated Receptor-2 Activation: A New Mechanism of Endothelial Dysfunction.Journal of the American Society of Nephrology : JASN · 2016Article
- New insights into sodium transport regulation in the distal nephron: Role of G-protein coupled receptors.World journal of biological chemistry · 2016Review
- The emerging role of coagulation proteases in kidney disease.Nature reviews. Nephrology · 2016Review
- Pathway-selective antagonism of proteinase activated receptor 2.British journal of pharmacology · 2014Article
- Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014Review
- Modulating human proteinase activated receptor 2 with a novel antagonist (GB88) and agonist (GB110).British journal of pharmacology · 2012Article
- PR3 and elastase alter PAR1 signaling and trigger vWF release via a calcium-independent mechanism from glomerular endothelial cells.PloS one · 2012Article
- Interleukin-17A promotes early but attenuates established disease in crescentic glomerulonephritis in mice.The American journal of pathology · 2011Article
- Blood pressures, heart rate and locomotor activity during salt loading and angiotensin II infusion in protease-activated receptor 2 (PAR2) knockout mice.BMC physiology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protease-activated receptor-2 (PAR-2) is a cellular receptor expressed prominently on epithelial, mesangial, and endothelial cells in the kidney and on macrophages. PAR-2 is activated by serine proteases such as trypsin, tryptase, and coagulation factors VIIa and Xa. It induces pleiotropic effects including vasodilatation, increasing plasminogen activator inhibitor (PAI-1) expression, mesangial cell proliferation, and cytokine production by macrophages. The role of PAR-2 in renal inflammation was studied in antiglomerular basement membrane antibody-induced crescentic glomerulonephritis (CGN) using PAR-2-deficient (PAR-2(-/-)) mice and wild-type littermate controls. PAR-2(-/-) mice had reduced crescent formation, proteinuria, and serum creatinine compared with wild-type mice 21 days after initiation of CGN. Glomerular accumulation of CD4(+) T cells and macrophages and the number of proliferating cells in glomeruli were similar in both groups. Glomerular fibrin deposition was significantly reduced in PAR-2(-/-) mice, and this was associated with reduced renal plasminogen activator inhibitor expression and increased renal matrix-metalloprotinase-9 activity. These results demonstrate a proinflammatory role for PAR-2 in CGN that is independent of effects on glomerular leukocyte recruitment and mesangial cell proliferation. PAR-2-mediated augmentation of renal plasminogen activator inhibitor expression and inhibition of matrix-metalloprotinase-9 activity may contribute to increased glomerular fibrin accumulation and glomerular injury in CGN.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.