Author/Authors :
Ge، نويسنده , , Ruiliang and Tai، نويسنده , , Yilin and Sun، نويسنده , , Yuanyuan and Zhou، نويسنده , , Kechun and Yang، نويسنده , , Shenglian and Cheng، نويسنده , , Tianlin and Zou، نويسنده , , Qifei and Shen، نويسنده , , Feng and Wang، نويسنده , , Yizheng، نويسنده ,
Abstract :
Intracellular Ca2+ signaling plays critical roles in VEGF-mediated angiogenesis. Transient receptor potential canonical (TRPC) channel 6, a Ca2+-permeable non-selective cation channel, can be activated by VEGF. Here, we report that TRPC6 is important for VEGF-mediated angiogenesis. Inhibition of TRPC6 in human umbilical vein endothelial cells (HUVECs) by pharmacological or genetic approaches arrested HUVECs at G2/M phase and suppressed VEGF-induced HUVEC proliferation and tube formation. Furthermore, inhibition of TRPCs abolished VEGF-, but not FGF-induced angiogenesis in the chick embryo chorioallantoic membrane. These results suggest that TRPC6 plays an important role in VEGF-mediated angiogenesis.
Keywords :
Angiogenesis , TRPC6 , VEGF , Proliferation , Tube formation
