Bisphenol A exposure stimulates prostatic fibrosis via exosome-triggered epithelium changes

Fibrosis is the pathological basis for the clinical progression of benign prostatic hyperplasia (BPH). Prostatic fibrosis is an important risk factor in patients with BPH who experience lower urinary tract symptoms. Bisphenol A (BPA) is an environmental endocrine disruptor (EED) that causes prostate defects. The effects of BPA on the prostate were investigated in this study using mouse and human prostate cell models. BPA-induced mouse prostatic fibrosis is characterized by collagen deposition and an increase in hydroxyproline concentration. Furthermore, BPA-exposed prostatic stromal fibroblasts exosomes promote the epithelial-mesenchymal transition of epithelial cells. High-throughput RNA sequencing and functional enrichment analyses show that substantially altered mRNAs, lncRNAs and circRNAs play roles in cellular interactions and the hypoxia-inducible factor-1 signaling pathway. The results showed that exosomes participated in the pro-fibrogenic effects of BPA on the prostate by mediating communication between stromal and epithelial cells and triggering epithelial changes. [Display omitted] •Bisphenol A exposure promoted prostatic epithelial-mesenchymal transition (EMT).•The prostate epithelial cells took in stromal cells-derived exosomes.•The exosomes promoted prostate epithelial cells collagen deposition and EMT.•Bisphenol A affected the exosomes profiles of circRNAs, lncRNAs and mRNAs.•Differentially expressed circRNAs and mRNAs participated HIF-1 signaling pathway.