最近研究发现PCOS发病机制可能与TGFβ信号通路相关。雄激素增多是PCOS发病机制的关键因素，然而TGFβ信号通路与雄激素增多的关系未明确。本课题组前期研究发现TGFβ超家族成员GDF9可抑制卵泡膜细胞雄激素的合成，推测 TGFβ信号通路可能与雄激素合成相关。本项目先以体外培养的人卵泡膜细胞为对象，通过免疫共沉淀技术、免疫印迹法识别GDF9的TGFβ信号通路，并抑制TGFβ信号通路功能观察雄激素合成的变化，以明确TGFβ信号通路在雄激素合成调节中的作用；然后通过免疫印迹法、ELISA法观察PCOS卵泡膜细胞中TGFβ信号通路表达的特点，并抑制TGFβ信号通路的功能观察PCOS卵泡膜细胞雄激素合成的变化，以明确TGFβ信号通路与PCOS卵泡膜细胞雄激素增多的关系。本项目旨在为阐明TGFβ信号通路在PCOS发病机制中的作用提供可靠证据，为进一步研究PCOS发病机制提供理论依据。

Recent studies have found that TGFβ signaling may be involved in pathogenesis of PCOS. However, it is not clear whether TGFβ signaling is related with hyperandrogenism which is a key factor in PCOS pathogenesis. In our previous study, we found that GDF9, a TGFβ superfamily member, can inhibit androgen production in theca cells, indicating TGFβ signaling may be involved in regulation of androgen production. In present study we firstly sought to identify the TGFβ signaling pathway of GDF9 in human theca cells by co-immunoprecipitation and immunoblotting and observe the change of androgen production after blockage of TGFβ signaling, in order to illustrate the role of TGFβ signaling in regulation of androgen production; then we intends to observe the expression patterns of TGFβ signaling pathway by immunoblotting and ELISA and observe the change of androgen production after blockage of TGFβ signaling in PCOS theca cells, in order to elucidate the relationship between TGFβ signaling and hyperandrogenism of PCOS. This project aims to provide reliable evidences for the role of TGFβ signaling in PCOS pathogenesis and theoretical basis for further research in pathogenesis mechanism of PCOS.