ArticleArthritis and rheumatism2012
Role of plasma kallikrein-kinin system activation in synovial recruitment of endothelial progenitor cells in experimental arthritis.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Pain mechanism and management strategy of rheumatoid arthritis.Frontiers in pain research (Lausanne, Switzerland) · 2025Review
- C1 inhibitor and prolylcarboxypeptidase modulate prekallikrein activation on endothelial cells.The Journal of allergy and clinical immunology · 2023Article
- Plasma Kallikrein as a Modulator of Liver Injury/Remodeling.Frontiers in pharmacology · 2021Article
- Increased fibrinolysis-induced bradykinin formation in hereditary angioedema confirmed using stored plasma and biotechnological inhibitors.BMC research notes · 2019Article
- A Combined Transcriptomic and Genomic Analysis Identifies a Gene Signature Associated With the Response to Anti-TNF Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2019Article
- The Plasma Kallikrein-Kininogen Pathway Is Critical in the Pathogenesis of Colitis in Mice.Frontiers in immunology · 2018Article
- Comparing Pathways of Bradykinin Formation in Whole Blood From Healthy Volunteers and Patients With Hereditary Angioedema Due to C1 Inhibitor Deficiency.Frontiers in immunology · 2018Article
- Plasma Prekallikrein: Its Role in Hereditary Angioedema and Health and Disease.Frontiers in medicine · 2018Review
- A critical role for plasma kallikrein in the pathogenesis of autoantibody-induced arthritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- An essential role of high-molecular-weight kininogen in endotoxemia.The Journal of experimental medicine · 2017Article
- Contact pathway of coagulation and inflammation.Thrombosis journal · 2015Article
- Kallikrein-kinin in stem cell therapy.World journal of stem cells · 2014Review
- A role for bradykinin in the development of anti-collagen antibody-induced arthritis.Rheumatology (Oxford, England) · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveTo examine whether activation of the plasma kallikrein-kinin system (KKS) mediates synovial recruitment of endothelial progenitor cells (EPCs) in arthritis.
methodsEPCs were isolated from Lewis rat bone marrow, and expression of progenitor cell-lineage markers and functional properties were characterized. EPCs were injected intravenously into Lewis rats with arthritis, and their recruitment and formation of de novo blood vessels in inflamed synovium were evaluated. The role of plasma KKS was examined using a plasma kallikrein inhibitor (EPI-KAL2) and an antikallikrein antibody (13G11). A transendothelial migration assay was used to determine the role of bradykinin and its receptor in EPC mobilization.
resultsEPCs from Lewis rats exhibited a strong capacity to form tubes and vacuoles and expressed increased levels of bradykinin type 2 receptor (B2R) and progenitor cell markers CD34 and Sca-1. In Lewis rats with arthritis, EPCs were recruited into inflamed synovium at the acute phase of disease and formed de novo blood vessels. Inhibition of plasma kallikrein by EPI-KAL2 and 13G11 significantly suppressed synovial recruitment of EPCs and hyperproliferation of synovial cells. Bradykinin stimulated transendothelial migration of EPCs in a concentration-dependent manner. This was mediated by B2R, as demonstrated by the finding that knockdown of B2R with silencing RNA completely blocked bradykinin-stimulated transendothelial migration. Moreover, bradykinin selectively up-regulated expression of the homing receptor CXCR4 in EPCs.
conclusionThese observations demonstrate a novel role of plasma KKS activation in the synovial recruitment of EPCs in arthritis, acting via kallikrein activation and B2R-dependent mechanisms. B2R might be involved in the mobilization of EPCs via up-regulation of CXCR4.
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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.