Yap/Taz Deletion in Gli⁺ Cell-Derived Myofibroblasts Attenuates Fibrosis.

ABSTRACT: In damaged kidneys, increased extracellular matrix (ECM) and tissue stiffness stimulate kidney fibrosis through incompletely characterized molecular mechanisms. The transcriptional coactivators yes-associated protein (Yap) and transcriptional coactivator with PDZ-binding motif (Taz) function as mechanosensors in cancer cells and have been implicated in the regulation of myofibroblasts in the kidney. We hypothesized that the development of kidney fibrosis depends on Yap-induced activation and proliferation of kidney fibroblasts. In mice, Yap expression increased in renal fibroblasts after unilateral ureteral obstruction (UUO), in association with worsening of interstitial fibrosis. In cultured fibroblasts, inhibition of Yap/Taz signaling blocked TGF-β1-induced fibroblast-to-myofibrob

SUBMITTER: Liang M 

PROVIDER: S-EPMC5661271 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature