TMEM16A drives renal cyst growth by augmenting Ca²⁺ signaling in M1 cells.

ABSTRACT: Polycystic kidney disease (PKD) leads to continuous decline of renal function by growth of renal cysts. Enhanced proliferation and transepithelial chloride secretion through cystic fibrosis transmembrane conductance regulator (CFTR) and Ca²⁺-activated TMEM16A Cl^- channels is thought to cause an increase in cyst volume. Recent work shows the pro-proliferative role of the Ca²⁺ activated Cl^- channel TMEM16A (anoctamin 1), and demonstrates the essential contribution of TMEM16A to CFTR-dependent Cl^- secretion. The present data demonstrate an increase in intracellular Ca²⁺ ([Ca²⁺]i) signals and Cl^- secretion by TMEM16A, in renal collecting duct principle cells from dog (MDCK) and mouse (M1) as well as primary

SUBMITTER: Cabrita I 

PROVIDER: S-EPMC7220898 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature