Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Wujin Road 85, Shanghai, 200080, China.
Shenzhen Institute of Translational Medicine, the First Affiliated Hospital of Shenzhen University, Shenzhen, 518035, China.
Biol Direct. 2024 Aug 2;19(1):61. doi: 10.1186/s13062-024-00504-y.
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.
肌成纤维细胞的堆积和前列腺纤维化在良性前列腺增生（BPH）的发展中起着关键作用。专门针对肌成纤维细胞的治疗方法可能是治疗 BPH 的一种有前途的方法。他达拉非是一种磷酸二酯酶 5（PDE5）抑制剂，有可能干预这一生物学过程。本研究利用前列腺基质成纤维细胞通过 TGFβ1 刺激诱导肌成纤维细胞分化。结果表明，与对照组相比，他达拉非显著抑制了前列腺基质成纤维细胞的增殖和纤维化过程。此外，我们的转录组测序结果表明，他达拉非通过抑制 TGFβ1 抑制 FGF9 的分泌，同时改善 miR-3126-3p 的表达。总的来说，TGFβ1 可以通过前列腺基质中的 miR-3126-3p 触发促纤维化信号，而他达拉非的使用可以抑制这一过程。
Zotero 插件
