P53 mutation regulates PKD genes and results in co-occurrence of PKD and tumorigenesis.

ABSTRACT:

Objective

Polycystic kidney disease (PKD) is the major cause of kidney failure and mortality in humans. It has always been suspected that the development of cystic kidney disease shares features with tumorigenesis, although the evidence is unclear.

Methods

We crossed p53 mutant mice (p53N236S, p53S) with Werner syndrome mice and analyzed the pathological phenotypes. The RNA-seq, ssGSEA analysis, and real-time PCR were performed to dissect the gene signatures involved in the development of disease phenotypes.

Results

We found enlarged kidneys with fluid-filled cysts in offspring mice with a genotype of G3mTerc ^-/- WRN ^-/- p53 ^S/S (G3TM). Pathology analysis confirmed the occurrence of PKD, and it was highly correlate

SUBMITTER: Li H 

PROVIDER: S-EPMC6528458 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature