ArticleArthritis research & therapy2008
Essential role of platelet activation via protease activated receptor 4 in tissue factor-initiated inflammation.
Article in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Protease-activated receptors act as a liaison between metabolism and inflammation.Inflammopharmacology · 2026Review
- Role of protease-activated receptor 4 in mouse models of acute and chronic kidney injury.American journal of physiology. Renal physiology · 2024Article
- Preliminary Study on Gene Regulation and its Pathways in Chinese Holstein Cows with Clinical Mastitis Caused byJournal of veterinary research · 2022Article
- Antioxidant and Anti-Inflammatory Effects ofFoods (Basel, Switzerland) · 2021Article
- Exploring Diagnostic Biomarkers and Comorbid Pathogenesis for Osteoarthritis and Metabolic Syndrome via Bioinformatics Approach.International journal of general medicine · 2021Article
- Using PAR4 Inhibition as an Anti-Thrombotic Approach: Why, How, and When?International journal of molecular sciences · 2019Review
- Proteinases and their receptors in inflammatory arthritis: an overview.Nature reviews. Rheumatology · 2018Review
- Effects ofBioMed research international · 2018Article
- Protease-activated receptor 4: from structure to function and back again.British journal of pharmacology · 2016Review
- Evolution of the protease-activated receptor family in vertebrates.International journal of molecular medicine · 2016Article
- Review
- Equine herpesvirus type 1 infection induces procoagulant activity in equine monocytes.Veterinary research · 2013Article
- Prothrombotic markers in patients with acute myocardial infarction and left ventricular thrombus formation treated with pci and dual antiplatelet therapy.Thrombosis journal · 2013Article
- Platelets: active players in the pathogenesis of arthritis and SLE.Nature reviews. Rheumatology · 2012Review
- Article
- Tissue factor, blood coagulation, and beyond: an overview.International journal of inflammation · 2011Article
- Deficiency of PAR4 attenuates cerebral ischemia/reperfusion injury in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010Article
- Novel aspects of fibrin(ogen) fragments during inflammation.Molecular medicine (Cambridge, Mass.)Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTissue factor (TF) activation of the coagulation proteases enhances inflammation in animal models of arthritis and endotoxemia, but the mechanism of this effect is not yet fully understood - in particular, whether this is primarily due to fibrin formation or through activation of protease activated receptors (PARs).
methodsWe induced extravascular inflammation by injection of recombinant soluble murine TF (sTF1-219) in the hind paw. The effects of thrombin inhibition, fibrinogen and platelet depletion were evaluated, as well as the effects of PAR deficiency using knockout mice deficient for each of the PARs.
resultsInjection of soluble TF provoked a rapid onset of paw swelling. Inflammation was confirmed histologically and by increased serum IL-6 levels. Inflammation was significantly reduced by depletion of fibrinogen (P < 0.05) or platelets (P = 0.015), and by treatment with hirudin (P = 0.04) or an inhibitor of activated factor VII (P < 0.001) compared with controls. PAR-4-deficient mice exhibited significantly reduced paw swelling (P = 0.003). In contrast, a deficiency in either PAR-1, PAR-2 or PAR-3 did not affect the inflammatory response to soluble TF injection.
conclusionOur results show that soluble TF induces acute inflammation through a thrombin-dependent pathway and both fibrin deposition and platelet activation are essential steps in this process. The activation of PAR-4 on platelets is crucial and the other PARs do not play a major role in soluble TF-induced inflammation.
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