miR-202-5p靶向AMH信号促进山羊卵泡优势化的分子机制研究

卵泡优势化对哺乳动物排卵至关重要，但卵泡优势化生长的分子机制尚未完全解析。申请人前期研究发现，miR-202-5p的表达量随着山羊卵泡生长而逐渐增加，并在优势卵泡中显著上调。预测发现miR-202-5p可靶向卵泡优势化负调控因子AMH的下游效应基因ACVR1和SMAD5等，提示其可能通过靶向抑制AMH信号通路促进山羊卵泡优势化。基于此，本项目通过检测miR-202-5p及AMH信号通路相关基因在不同发育阶段的山羊卵泡中时空表达模式；随后，在体外培养的山羊有腔卵泡中，研究过表达或干扰miR-202-5p对卵泡发育中AMH信号传递的影响；最后，在卵泡颗粒细胞中，过表达或干扰靶基因ACVR1和SMAD5，探究miR-202-5p靶向AMH信号通路调控卵泡优势化的分子机制。本研究将初步解析miR-202-5p在卵泡发育及卵泡优势化中的分子机理，以期提高卵巢排卵数，为改善山羊繁殖性能提供理论依据。

The follicular dominance of mammalian is crucial to ovulation, but the molecular mechanisms of dominant follicles selection is still elusive. Our previous studies have shown that miR-202-5p was significantly enriched in dominant follicles and its expression increased with follicle growth. It was also found that miR-202-5p could directly target several key genes that involved in AMH signaling, ACVR1 and SMAD5. AMH was proved to be a negative regulate factor of follicular dominance. Therefore, we hypothesized that miR-202-5p may promote the follicle dominance by inhibiting AMH signaling. In this study, we will carry out the following research: (1) Identification of the expression and location of miR-202-5p and the target genes in AMH signaling in different follicular stages. (2) Explore the signal transmission of AMH in follicle growth that effect by miR-202-5p through overexpress or interfere miR-202-5p in cultured goat antral follicles in vitro. (3) Study the molecular mechanism of miR-202-5p targeting AMH signaling through up/down regulate the expression of ACVR1 and SMAD5 in goat granulosa cells. This study will preliminarily resolve the molecular mechanism of miR-202-5p in follicular development and the dominance in goats. The results will provide a theoretical basis for promoting ovulation rate and improving the reproductive performance of goats.