1. Academic Validation
  2. Phosphodiesterase type 5 inhibitor tadalafil reduces prostatic fibrosis via MiR-3126-3p/FGF9 axis in benign prostatic hyperplasia

Phosphodiesterase type 5 inhibitor tadalafil reduces prostatic fibrosis via MiR-3126-3p/FGF9 axis in benign prostatic hyperplasia

  • Biol Direct. 2024 Aug 2;19(1):61. doi: 10.1186/s13062-024-00504-y.
Tiewen Li # 1 Yu Zhang # 1 Zeng Zhou # 1 Lvxin Guan 2 Yichen Zhang 1 Zhiyuan Zhou 3 Wenhao Wang 1 Xuehao Zhou 1 Di Cui 4 Chenyi Jiang 5 Yuan Ruan 6
Affiliations

Affiliations

  • 1 Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Wujin Road 85, Shanghai, 200080, China.
  • 2 Shenzhen Institute of Translational Medicine, the First Affiliated Hospital of Shenzhen University, Shenzhen, 518035, China.
  • 3 Department of Urology, Shanghai Pudong New Area GongLi Hospital, 219 Miaopu Road, Shanghai, 200135, China.
  • 4 Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Wujin Road 85, Shanghai, 200080, China. cuidi2001@126.com.
  • 5 Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Wujin Road 85, Shanghai, 200080, China. chenyi.jiang@shgh.cn.
  • 6 Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Wujin Road 85, Shanghai, 200080, China. yuanruan@163.com.
  • # Contributed equally.
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.

Keywords

Benign prostatic hyperplasia; FGF9; Myofibroblast differentiation; Phosphodiesterase 5 inhibitor; miR-3126-3p.

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