Mouse transient receptor potential channel 6: role in hemostasis and thrombogenesis. Academic Article uri icon


  • Although changes in the intracellular levels of calcium (Ca(2+)) are a central step in platelet activation, the underlying mechanism of Ca(2+) entry is still unclear. Previous studies have demonstrated that TRPC6, a member of the canonical transient receptor potential channel (TRPC) family is expressed in platelets in a significant amount, and is predominantly found on the plasma membrane. Based on these considerations, we hypothesized that TRPC6 plays a critical role in platelet function. To characterize the role of TRPC6 in platelet function in vivo, we employed a genetic approach, subjecting TRPC6 knockout mice to the tail bleeding time test and a carotid artery injury thrombosis model. We found that TRPC6-deficient animals displayed a prolonged bleeding time, and an increased time for occlusion of the injured carotid artery, compared to their wild-type littermates. Taken together, our data demonstrate for the first time, that TRPC6 deletion in mice results in defects in hemostasis and protection against thrombogenesis, suggesting a vital role in platelet function. Furthermore, TRPC6 may define a new therapeutic target for managing multiple thrombosis-based disorders.

published proceedings

  • Biochem Biophys Res Commun

author list (cited authors)

  • Paez Espinosa, E. V., Murad, J. P., Ting, H. J., & Khasawneh, F. T.

citation count

  • 27

complete list of authors

  • Paez Espinosa, Enma V||Murad, John P||Ting, Harold J||Khasawneh, Fadi T

publication date

  • January 2012