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Cl-Inhibitor Decreases the Release of Vasculitis-Like Chemotactic Endothelial Microvesicles
Lund University, Sweden.
Lund University, Sweden.
Lund University, Sweden.
Lund University, Sweden.
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2017 (English)In: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 28, no 8, p. 2472-2481Article in journal (Refereed) Published
Abstract [en]

The kinin system is activated during vasculitis and may contribute to chronic inflammation. C1-inhibitor is the main inhibitor of the kinin system. In this study, we investigated the presence of the kinin B1 receptor on endothelial microvesicles and its contribution to the inflammatory process. Compared with controls (n=15), patients with acute vasculitis (n=12) had markedly higher levels of circulating endothelial micro vesicles, identified by flow cytometry analysis, and significantly more microvesicles that were positive for the kinin B1 receptor (Pamp;lt;0.001). Compared with microvesicles from wild-type cells, B1 receptor-positive microvesicles derived from transfected human embryonic kidney cells induced a significant neutrophil chemotactic effect, and a B1 receptor antagonist blocked this effect. Likewise, patient plasma induced neutrophil chemotaxis, an effect decreased by reduction of microvesicle levels and by blocking the B1 receptor. We used a perfusion system to study the effect of patient plasma (n=6) and control plasma (n=6) on the release of microvesicles from glomerular endothelial cells. Patient samples induced the release of significantly more B1 receptor-positive endothelial microvesicles than control samples, an effect abrogated by reduction of the microvesicles in the perfused samples. Perfusion of C1-inhibitor depleted plasma over glomerular endothelial cells promoted excessive release of B1 receptor-positive endothelial microvesicles compared with normal plasma, an effect significantly decreased by addition of C1-inhibitor or B1 receptor-antagonist. Thus, B1 receptor-positive endothelial microvesicles may contribute to chronic inflammation by inducing neutrophil chemotaxis, and the reduction of these microvesicles by C1-inhibitor should be explored as a potential treatment for neutrophil-induced inflammation.

Place, publisher, year, edition, pages
AMER SOC NEPHROLOGY , 2017. Vol. 28, no 8, p. 2472-2481
National Category
Urology and Nephrology
Identifiers
URN: urn:nbn:se:liu:diva-139909DOI: 10.1681/ASN.2016060637ISI: 000406570500021PubMedID: 28289183OAI: oai:DiVA.org:liu-139909DiVA, id: diva2:1135740
Note

Funding Agencies|Swedish Research Council [K2013-64X-14008-13-5, K2015-99X-22877-01-6]; Knut and Alice Wallenberg Foundation [2015.0320]; Torsten Soderberg Foundation; Skine Centre of Excellence in Health; IngaBritt och Arne Lundbergs Research Foundation; Crown Princess Lovisas Society for Child Care Region Skane; Konung Gustaf V:s 80-arsfond; Alfred Osterlund Foundation; Swedish Rheumatism Association; Medical Faculty of the University of Lund; Anna-Greta Crafoord Foundation; Greta and Johan Kocks Foundation; Samariten Foundation; Fanny Ekdahl Foundation; Jerring Foundation; Thelma Zoegas Foundation

Available from: 2017-08-24 Created: 2017-08-24 Last updated: 2017-08-24

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Segelmark, Mårten
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Division of Drug ResearchFaculty of Medicine and Health SciencesDepartment of Nephrology
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