卵母细胞减数分裂阻滞与促黄体素诱导减数分裂恢复的分子机制研究进展

Advances in molecular mechanisms of meiotic arrest and luteinizing hormoneinduced meiotic resumption in oocytes

哺乳动物排卵前,卵泡中的卵母细胞一直被阻滞在减数分裂I前期的双线期,卵泡壁层颗粒细胞分泌的C型利尿钠肽(C-type natriuretic peptide, NPPC)与表达在卵丘细胞中的同源利尿钠肽受体2 (natriuretic peptide receptor 2, NPR2)结合,产生的cGMP是维持减数分裂阻滞的关键因子。另外,cAMP、缝隙连接、肌苷单磷酸脱氢酶(inosine monophosphate dehydrogenase,IMPDH)等多种重要调控因子也参与了减数分裂阻滞。当垂体分泌的促黄体素(luteinizing hormone, LH)峰到来时,LH通过多种调控方式迅速降低胞内cGMP水平,使卵母细胞恢复减数分裂。本文对维持卵母细胞减数分裂I阻滞以及LH诱导减数分裂恢复的机制研究进展进行综述,为相关生殖疾病的预防和诊治提供思路。

Mammalian oocytes within Graafian follicles are arrested at prophase I of meiosis. C-type natriuretic peptide(NPPC), secreted by mural granulosa cells(MGCs), maintains oocyte meiotic arrest via binding to its cognate receptor natriuretic peptide receptor 2(NPR2) and producing cyclic guanosine monophosphate(cGMP). NPR2 is most concentrated in the cumulus cells. In addition, cAMP, gap junction, inosine monophosphate dehydrogenase(IMPDH) and other important regulatory factors are also involved in meiotic arrest. Luteinizing hormone(LH) then rapidly decreases cGMP and induces oocyte meiotic resumption. In this paper, advances in the molecular mechanisms of meiotic arrest and LH-induced meiotic resumption were reviewed. This paper may provide new ideas for the prevention, diagnosis and treatment of related reproductive diseases.