Tubular STAT3 Limits Renal Inflammation in Autosomal Dominant Polycystic Kidney Disease.

ABSTRACT:

Background

The inactivation of the ciliary proteins polycystin 1 or polycystin 2 leads to autosomal dominant polycystic kidney disease (ADPKD). Although signaling by primary cilia and interstitial inflammation both play a critical role in the disease, the reciprocal interactions between immune and tubular cells are not well characterized. The transcription factor STAT3, a component of the cilia proteome that is involved in crosstalk between immune and nonimmune cells in various tissues, has been suggested as a factor fueling ADPKD progression.

Method

To explore how STAT3 intersects with cilia signaling, renal inflammation, and cyst growth, we used conditional murine models involving postdevelopmental ablation of Pkd1, Stat3, and cilia, as well as cultures of ci

SUBMITTER: Viau A 

PROVIDER: S-EPMC7217419 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature