Protein’s Role In Blood Clotting Differs In Vitro And In Vivo

The formation of a blood clot (also known as a thrombus) is a key step in stopping bleeding after tissue injury. The adhesion of platelets to a blood vessel wall and their subsequent aggregation and activation are essential for thrombus formation.

Previous in vitro studies have shown that a protein known as vWF is essential for platelet adhesion, aggregation, and activation in thrombus formation. However, researchers from the Beth Israel Deaconess Medical Center, Boston, have now shown that vWF is not required for in vivo platelet activation in mice in which tissue injury was induced with a laser.In the study, which appears online in advance of publication in the April print issue of the Journal of Clinical Investigation, Bruce Furie and colleagues show that in mice lacking vWF, platelet activation (as measured by calcium mobilization) occurred normally following laser-induced injury, although platelet adhesion and aggregation were impaired. Platelet activation following laser-induced injury was shown to occur via the tissue factor-mediated pathway and not the collagen-mediated pathway. Therefore, this study indicates that, surprisingly, vWF is not required for in vivo tissue factor-mediated platelet activation, although other studies have indicated that it might have an in vivo role in collagen-mediated platelet activation. (Source: Journal of Clinical Investigation : Beth Israel Deaconess Medical Center and Harvard Medical School : April 2007.)