Arteriosclerosis, Thrombosis, and Vascular Biology 2011-12-01

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

Julia Searle, Martin Mockel, Stefanie Gwosc, Saul A Datwyler, Fatimunnisa Qadri, Gesa I Albert, Fabian Holert, Annette Isbruch, Lars Klug, Dominik N Muller, Ralf Dechend, Reinhold Muller, Joern O Vollert, Anna Slagman, Christian Mueller, Florian Herse

文献索引：Arterioscler. Thromb. Vasc. Biol. 31(12) , 2972-4, (2011)

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摘要

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.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.Heparin releases sFlt1 by displacing the sFlt1 heparin-binding site from heparan sulfate proteoglycans. Heparin could induce an antiangiogenic state.