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The urothelium is an epithelial barrier lining the bladder that protects against infection, fluid exchange and damage from toxins. The nuclear receptor  Pparg  promotes urothelial differentiation in vitro, and  Pparg  mutations are associated with bladder cancer. However, the function of Pparg in the healthy urothelium is unknown. Here we show that  Pparg  is critical in urothelial cells for mitochondrial biogenesis, cellular differentiation and regulation of inflammation in response to urinary tract infection (UTI). Superficial cells, which are critical for maintaining the urothelial barrier, fail to mature in  Pparg  mutants and basal cells undergo squamous-like differentiation.  Pparg  mutants display persistent inflammation after UTI, and Nf-KB, which is transiently activated in response to infection in the wild type urothelium, persists for months. Our observations suggest that in addition to its known roles in adipogegnesis and macrophage differentiation, that Pparg-dependent transcription plays a role in the urothelium controlling mitochondrial function development and regeneration.

Pparg promotes differentiation and regulates mitochondrial gene expression in bladder epithelial cells