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Scripps Research team sheds new light on how blood clots form
Date:6/13/2011

functional P2X7 receptors, and found that these P2X7-knockout mice failed to form stable arterial blood clots when the vessel wall was exposed to a clot-inducing substance. Importantly, these mice did not suffer from uncontrollable bleeding. "This suggests that clot-preventing drugs targeting the P2X7 pathway might not have unacceptable side effects," said Ruf.

In the cell experiments, the team found that the cascade of molecular events following P2X7 stimulation alters the activity of a thiol-targeting enzyme known as protein disulfide isomerase (PDI), which Ruf's previous studies had implicated as a possible activator of tissue factor. In the new study, the scientists demonstrated the importance of PDI in this process by showing that they could block clot formation in normal mice with anti-PDI antibodies.

Targeting the top of the clot-formation pathway by blocking the P2X7 receptor might have even broader beneficial effects, since the activation of this receptor occurs in a number of inflammatory disorders.

"Cardiovascular disease and heart attacks are caused by chronic inflammation as well as clot formation," said Ruf, "so possibly P2X7 is a major explanation for the link between inflammation and thrombosis, as well as a good target for preventing these conditions."


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Contact: Mika Ono
mikaono@scripps.edu
858-784-2052
Scripps Research Institute
Source:Eurekalert

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