3 years ago

The TRPC5 channel regulates angiogenesis and promotes recovery from ischemic injury in mice.

Yifei Zhu, Mengru Gao, Tingting Zhou, Mingxu Xie, Aiqin Mao, Lei Feng, Xiaoqiang Yao, Wing Tak Wong, xin Ma
Ischemia-related diseases are a leading cause of death worldwide, and promoting therapeutic angiogenesis is key to effective recovery from hypoxia-ischemia. Given the limited success of angiogenic factors, such as vascular endothelial growth factor, in clinical trials, it is important to find more promising angiogenic targets. Here, using both cell- and tissue-based assays and a mouse model of injury-induced ischemia, we investigated the involvement of the transient receptor potential canonical 5 (TRPC5) ion channel in angiogenesis and the effects of a TRPC5 activator, the FDA-approved drug riluzole, on recovery from ischemic injury. We demonstrate that TRPC5 is involved in endothelial cell sprouting, angiogenesis and blood perfusion in an oxygen-induced retinopathy model and a hind-limb ischemia model. We found a potential regulatory link between nuclear factor of activated T cell isoform c3 and angiopoietin-1 that could provide the mechanistic basis for the angiogenic function of TRPC5. Importantly, treatment with riluzole, which can activate TRPC5 in endothelial cells, improved recovery from ischemia in mice. Our study reveals TRPC5 as a potential angiogenic target and suggests riluzole as a promising drug for managing ischemic diseases.

Publisher URL: http://doi.org/10.1074/jbc.RA118.005392

DOI: 10.1074/jbc.RA118.005392

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