多囊卵巢综合征(PCOS)是最常见的由于排卵障碍导致不孕的生殖内分泌疾病，发病率在育龄女性约为10％。有证据表明颗粒细胞增殖-凋亡平衡调控对于PCOS病理发生等过程具有极其重要的影响。我们前期的研究中证实颗粒细胞内microRNA参与颗粒细胞增殖、分化等关键过程，并且发现颗粒细胞内miR-483-5P及其下游靶基因ERK1可能在PCOS的发生、发展过程中发挥重要调控作用，值得进一步探讨。本课题旨在前期研究的基础上，证实miR-483-5P通过靶基因ERK1及其下游MAPK通路参与调节颗粒细胞的增殖-凋亡平衡，并结合人类PCOS颗粒细胞和PCOS大鼠模型，阐明miR-483-5P及其下游通路参与PCOS发生的具体分子机制。希望丰富miRNA在卵泡、卵巢生理发育和PCOS等病理发生、发展中的研究资料，并为未来PCOS等相关疾病的临床诊疗中提供新的思路及潜在靶点。

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder found in women. PCOS produces symptoms in approximately 5% to 10% of women on reproductive age, and it is thought to be one of the leading causes of female sub-fertility. The principal features are excessive amounts of androgenic hormones and anovulation. It has been reported that proliferation-apoptosis balance of granulosa cells affected the development of oocytes, follicles and embryos in patients with PCOS. In our previous reports, we miRNAs and their targeted pathways play important roles granulosa cells. Moreover, miR-483-5p were found to be involved in the regulation of etiology and pathophysiology of PCOS. Therefore, we aimed to describe the regulation role of miR-483-5P and its targeted gene-ERK1 in proliferation-apoptosis balance of granulosa cells and development of PCOS based on isolation human PCOS granulosa cells and PCOS rat model. These results will be useful for understanding development of oocytes, follicles and embryos, and for the pathologic development of PCOS, and provides novel candidates for molecular biomarkers or treatment targets in the research of female infertility associated with PCOS.