Gender-Dependent Phenotype in Polycystic Kidney Disease Is Determined by Differential Intracellular Ca²⁺ Signals.

ABSTRACT: Autosomal dominant polycystic kidney disease (ADPKD) is caused by loss of function of PKD1 (polycystin 1) or PKD2 (polycystin 2). The Ca²⁺-activated Cl^- channel TMEM16A has a central role in ADPKD. Expression and function of TMEM16A is upregulated in ADPKD which causes enhanced intracellular Ca²⁺ signaling, cell proliferation, and ion secretion. We analyzed kidneys from Pkd1 knockout mice and found a more pronounced phenotype in males compared to females, despite similar levels of expression for renal tubular TMEM16A. Cell proliferation, which is known to be enhanced with loss of Pkd1^-/-, was larger in male when compared to female Pkd1^-/- cells. This was paralleled by higher basal intracellular Ca²⁺ concentrations in primary

SUBMITTER: Talbi K 

PROVIDER: S-EPMC8199720 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature