Non-Cell-Autonomous Regulation of Prostate Epithelial Homeostasis by Androgen Receptor.
Ontology highlight
ABSTRACT: Prostate inflammation has been suggested as an etiology for benign prostatic hyperplasia (BPH). We show that decreased expression of the androgen receptor (AR) in luminal cells of human BPH specimens correlates with a higher degree of regional prostatic inflammation. However, the cause-and-effect relationship between the two events remains unclear. We investigated specifically whether attenuating AR activity in prostate luminal cells induces inflammation. Disrupting luminal cell AR signaling in mouse models promotes cytokine production cell-autonomously, impairs epithelial barrier function, and induces immune cell infiltration, which further augments local production of cytokines and chemokines including Il-1 and Ccl2. This inflammatory microenvironment promotes AR-independent prostatic ep
SUBMITTER: Zhang B
PROVIDER: S-EPMC5026614 | biostudies-literature | 2016 Sep
REPOSITORIES: biostudies-literature
ACCESS DATA