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Heparin strongly induces soluble fms-like tyrosine kinase 1 release in vivo and in vitro

Item Type:Article
Title:Heparin strongly induces soluble fms-like tyrosine kinase 1 release in vivo and in vitro
Creators Name:Searle, J. and Mockel, M. and Gwosc, S. and Datwyler, S.A. and Qadri, F. and Albert, G.I. and Holert, F. and Isbruch, A. and Klug, L. and Mueller, D.N. and Dechend, R. and Muller, R. and Vollert, J.O. and Slagman, A. and Mueller, C. and Herse, F.
Abstract:OBJECTIVE: Soluble fms-like tyrosine kinase 1 (sFlt1) is involved in the pathophysiology of preeclampsia and coronary artery disease. Because sFlt1 has a heparin-binding site, we investigated whether or not heparin releases sFlt1 from the extracellular matrix. METHODS AND RESULTS: We measured sFlt1 before and after heparin administration in 135 patients undergoing coronary angiography, percutanous coronary intervention, or both. sFlt1 was increased directly after heparin administration (from 254 to 13 440 pg/mL) and returned to baseline within 10 hours. Umbilical veins and endothelial cells treated with heparin released sFlt1. Heparinase I and III also increased sFlt1. Mice treated with heparin had elevated sFlt1 serum levels. Their serum inhibited endothelial tube formation. CONCLUSIONS: Heparin releases sFlt1 by displacing the sFlt1 heparin-binding site from heparan sulfate proteoglycans. Heparin could induce an antiangiogenic state.
Keywords:Angiogenesis, Angiography, Coronary Artery Disease, Heparin, SFlt1, Animals, Mice
Source:Arteriosclerosis Thrombosis and Vascular Biology
Publisher:American Heart Association
Page Range:2972-2974
Date:December 2011
Official Publication:https://doi.org/10.1161/ATVBAHA.111.237784
PubMed:View item in PubMed

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