Mechanoprotection by polycystins against apoptosis is mediated through the opening of stretch-activated K(2P) channels.

ABSTRACT: How renal epithelial cells respond to increased pressure and the link with kidney disease states remain poorly understood. Pkd1 knockout or expression of a PC2 pathogenic mutant, mimicking the autosomal dominant polycystic kidney disease, dramatically enhances mechanical stress-induced tubular apoptotic cell death. We show the presence of a stretch-activated K(+) channel dependent on the TREK-2 K(2P) subunit in proximal convoluted tubule epithelial cells. Our findings further demonstrate that polycystins protect renal epithelial cells against apoptosis in response to mechanical stress, and this function is mediated through the opening of stretch-activated K(2P) channels. Thus, to our knowledge, we establish for the first time, both in vitro and in vivo, a functional relationship between me

SUBMITTER: Peyronnet R 

PROVIDER: S-EPMC3437542 | biostudies-literature | 2012 Mar

REPOSITORIES: biostudies-literature