| Full text | |
| Author(s): |
Total Authors: 4
|
| Affiliation: | [1] Univ Estadual Campinas, UNICAMP, Inst Biol, Dept Anat Cellular Biol Physiol & Biophys, Sao Paulo - Brazil
[2] Blood Ctr Wisconsin, Milwaukee, WI - USA
[3] St Louis Univ, Dept Biochem, St Louis, MO 63103 - USA
[4] Washington Univ, Sch Med, Div Hematol, St Louis, MO 63110 - USA
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | THROMBOSIS RESEARCH; v. 130, n. 4, p. 646-648, OCT 2012. |
| Web of Science Citations: | 3 |
| Abstract | |
Introduction: The thrombin mutant W215A/E217A (WE thrombin) has greatly reduced procoagulant activity, but it activates protein C in the presence of thrombomodulin and inhibits binding of platelet glycoprotein Ib to von Willebrand factor and collagen under flow conditions. Both thrombomodulin-dependent protein C activation and inhibition of platelet adhesion could contribute to the antithrombotic activity of WE thrombin. Materials and methods: To assess the role of thrombomodulin, we administered WE thrombin to thrombomodulin-deficient (TMPro/Pro) mice and measured the time to occlusive thrombus formation in the carotid artery after photochemical injury of the endothelium. Results and conclusions: Doses of WE thrombin >= 10 mu g/kg prolonged the thrombosis time of wild-type mice (> 1.6-fold), while doses >= 100 mu g/kg only slightly prolonged the thrombosis time of TMPro/Pro mice. We conclude that thrombomodulin plays a predominate role in mediating the antithrombotic effect of WE thrombin in the arterial circulation of mice after endothelial injury. Thrombomodulin-independent effects may occur only when high doses of WE thrombin are administered. (c) 2011 Elsevier Ltd. All rights reserved. (AU) | |
| FAPESP's process: | 10/11474-5 - Influence of glycosaminoglycans in inflammation and cellular therapy using endothelial progenitor cells after arterial injury in mice |
| Grantee: | Cristina Pontes Vicente |
| Support Opportunities: | Regular Research Grants |