Dec. 21, 2009 Inappropriate activation of the blood clotting process inside a blood vessel results in the formation of a clot known as a thrombus. Thrombus formation in blood vessels in the brain and heart can lead to stroke and heart attack, respectively. Drugs that prevent blood clot formation reduce the risk of these conditions.
A team of researchers, at The University of Tokyo, Japan, and the International Medical Center of Japan, has now identified a role for the protein Lnk in stabilizing thrombus formation in mice, suggesting that it might provide a therapeutic target to prevent thrombus formation.
The research appears in the Journal of Clinical Investigation.
The team, led by Koji Eto and Satoshi Takaki, studied mice lacking Lnk and by imaging the process of thrombus formation in blood vessels found that Lnk played an essential role in stabilizing developing thrombi in blood vessels.
Further analysis revealed the key signaling pathway regulated by Lnk. As Lnk-deficient mice did not have a spontaneous bleeding problem, the authors suggest that targeting Lnk or other proteins in the pathway might provide therapeutic targets that provide less risk for bleeding than those targeted by conventional drugs.
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- Hitoshi Takizawa, Satoshi Nishimura, Naoya Takayama, Atsushi Oda, Hidekazu Nishikii, Yohei Morita, Sei Kakinuma, Satoshi Yamazaki, Satoshi Okamura, Noriko Tamura, Shinya Goto, Akira Sawaguchi, Ichiro Manabe, Kiyoshi Takatsu, Hiromitsu Nakauchi, Satoshi Takaki and Koji Eto. Lnk regulates integrin alpha-IIb-beta-3 outside-in signaling in mouse platelets, leading to stabilization of thrombus development in vivo. Journal of Clinical Investigation, 2009; DOI: 10.1172/JCI39503
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