1. Phosphodiesterase type 5 inhibitor tadalafil reduces prostatic fibrosis via MiR-3126-3p/FGF9 axis in benign prostatic hyperplasia
- Author
-
Tiewen Li, Yu Zhang, Zeng Zhou, Lvxin Guan, Yichen Zhang, Zhiyuan Zhou, Wenhao Wang, Xuehao Zhou, Di Cui, Chenyi Jiang, and Yuan Ruan
- Subjects
Benign prostatic hyperplasia ,Myofibroblast differentiation ,Phosphodiesterase 5 inhibitor ,miR-3126-3p ,FGF9 ,Biology (General) ,QH301-705.5 - Abstract
Abstract Myofibroblast buildup and prostatic fibrosis play a crucial role in the development of benign prostatic hyperplasia (BPH). Treatments specifically targeting myofibroblasts could be a promising approach for treating BPH. Tadalafil, a phosphodiesterase type 5 (PDE5) inhibitor, holds the potential to intervene in this biological process. This study employs prostatic stromal fibroblasts to induce myofibroblast differentiation through TGFβ1 stimulation. As a result, tadalafil significantly inhibited prostatic stromal fibroblast proliferation and fibrosis process, compared to the control group. Furthermore, our transcriptome sequencing results revealed that tadalafil inhibited FGF9 secretion and simultaneously improved miR-3126-3p expression via TGFβ1 suppression. Overall, TGFβ1 can trigger pro-fibrotic signaling through miR-3126-3p in the prostatic stroma, and the use of tadalafil can inhibit this process.
- Published
- 2024
- Full Text
- View/download PDF