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Activation of TRPV4 channels prevents angiogenesis.

Angiogenesis plays an important role in ischemic diseases, inflammation, wound healing, and tumor progression. Recent studies have demonstrated that transient receptor potential vanilloid 4 (TRPV4) channel, belonging to a Transient Receptor Potential (TRP) family of ion channels, regulates the cell survival and death in endothelial cells and tumor angiogenesis. In this study, we examined the effects of the TRPV4 channel agonist GSK1016790A on the cell survival and viability of human umbilical vein endothelial cells (HUVECs) and on retinal angiogenesis in neonatal mice. GSK1016790A (100 nM) increased the number of propidium iodide-positive cells and reduced the cell viability of HUVECs. Pre-treatment of HUVECs with the TRPV4 channel antagonist HC-067047 (1 μM) prevented GSK1016790A-induced reduction in the cell viability. Retinal angiogenesis was slightly delayed in mice treated with GSK1016790A (0.3 mg/kg, s.c.) from postnatal day (P) 2 to P5. These results suggest that an excessive activation of TRPV4 channels induces endothelial cell death and shows the anti-angiogenic effect. Thus, TRPV4 channels may be a target for anti-angiogenic intervention in ischemic diseases and tumor growth.