Arterioscler Thromb Vasc Biol. 2011 Dec;31(12):2972-4. Epub 2011 Oct 6.

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

Searle J, Mockel M, Gwosc S, Datwyler SA, Qadri F, Albert GI, Holert F, Isbruch A, Klug L, Muller DN, Dechend R, Muller R, Vollert JO, Slagman A, Mueller C, Herse F.

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Department of Cardiology, Campus Virchow Klinikum, Charité–Universitätsmedizin Berlin, Germany.

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.

PMID:: 21979436; [PubMed - indexed for MEDLINE]

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

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