Mouse transient receptor potential channel 6: Role in hemostasis and thrombogenesis

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

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

32 Citas (Scopus)


Although changes in the intracellular levels of calcium (Ca2+) are a central step in platelet activation, the underlying mechanism of Ca2+ 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.

Idioma originalInglés
Páginas (desde-hasta)853-856
Número de páginas4
PublicaciónBiochemical and Biophysical Research Communications
EstadoPublicada - 13 ene. 2012
Publicado de forma externa

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