随着社会老龄化进展，良性前列腺增生（BPH）严重影响老年男性的生活质量。课题组前期研究发现：前列腺增生时异常活化的TGF-β能募集间充质干细胞（MSCs）到前列腺间质，并诱导其定向分化为肌成纤维细胞，同时上调RhoA通路重要蛋白ROCK表达，继而推测TGF-β可能主要通过RhoA/ROCK信号通路影响MSCs募集和分化，参与BPH的发生发展。本课题将以小鼠前列腺组织的MSCs为研究对象，以多种转基因、基因敲除小鼠和连体鼠模型为研究工具，结合临床BPH患者手术标本，采用RhoA基因敲减或过表达技术、Transwell细胞募集系统、液相蛋白芯片检测、ROCK抑制剂干预、共聚焦显微镜观察、流式细胞仪检测等研究方法，从分子、细胞、活体水平探讨TGFβ通过RhoA/ROCK信号通路介导MSCs募集和定向分化在前列腺增生中的作用机制，为BPH的治疗提供新的方向和靶点。

With the progress of the aging society, benign prostatic hyperplasia (BPH) has a serious impact on the quality of life of the elderly men. Our preliminary study confirmed that aberrant activation of TGF-β resulted in the recruitment of mesenchymal stem cells (MSCs) and their subsequent differentiation into prostatic stromal cells during prostatic hyperplasia. Meanwhile, ROCK expression increased in the differentiation of MSCs induced by TGF-β. Thus, we speculated that TGF-β could recruit MSCs and promote myofibrogenic differentiation of MSCs through the RhoA/ROCK pathways. We will explore difference approaches and methods, such as RhoA overexpression and knockdown, cell signaling pathway blocking, Transwell in vitro recruitment system, transgenic and gene knockout mice, parabiosis mice model, confocal fluorescence microscope, flow cytometry and so on. We aims to prove that TGFβ recruits and determines lineage fate of MSCs by RhoA/ROCK signaling pathway during prostatic hyperplasia at molecular, cellular, and in vivo levels. This study might provide potential therapeutic options in the management of BPH.