Prothymosin α promotes STAT3 acetylation to induce cystogenesis in Pkd1-deficient mice.

ABSTRACT: Polycystic kidney disease (PKD) is characterized by the expansion of fluid-filled cysts in the kidney, which impair the function of kidney and eventually leads to end-stage renal failure. It has been previously demonstrated that transgenic overexpression of prothymosin α (ProT) induces the development of PKD; however, the underlying mechanisms remain unclear. In this study, we used a mouse PKD model that sustains kidney-specific low-expression of Pkd1 to illustrate that aberrant up-regulation of ProT occurs in cyst-lining epithelial cells, and we further developed an in vitro cystogenesis model to demonstrate that the suppression of ProT is sufficient to reduce cyst formation. Next, we found that the expression of ProT was accompanied with prominent augmentation of protein ac

SUBMITTER: Chen YC 

PROVIDER: S-EPMC6902686 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature