颗粒细胞配体 NPPC 及其受体 NPR2 维持小鼠卵母细胞减数分裂阻滞。
Granulosa cell ligand NPPC and its receptor NPR2 maintain meiotic arrest in mouse oocytes.
机构信息
State Key Laboratory for Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, People's Republic of China.
出版信息
Science. 2010 Oct 15;330(6002):366-9. doi: 10.1126/science.1193573.
Abstract
Granulosa cells of mammalian Graafian follicles maintain oocytes in meiotic arrest, which prevents their precocious maturation. We show that mouse mural granulosa cells, which line the follicle wall, express natriuretic peptide precursor type C (Nppc) messenger RNA (mRNA), whereas cumulus cells surrounding oocytes express mRNA of the NPPC receptor NPR2, a guanylyl cyclase. NPPC increased cGMP levels in cumulus cells and oocytes and inhibited meiotic resumption in vitro. Meiotic arrest was not sustained in most Graafian follicles of Nppc or Npr2 mutant mice, and meiosis resumed precociously. Oocyte-derived paracrine factors promoted cumulus cell expression of Npr2 mRNA. Therefore, the granulosa cell ligand NPPC and its receptor NPR2 in cumulus cells prevent precocious meiotic maturation, which is critical for maturation and ovulation synchrony and for normal female fertility.
摘要
哺乳动物的卵丘颗粒细胞维持减数分裂阻滞，防止卵母细胞过早成熟。我们发现，位于卵泡壁的小鼠壁颗粒细胞表达利钠肽前体 C（Nppc）信使 RNA（mRNA），而围绕卵母细胞的卵丘细胞表达 NPPC 受体 NPR2 的 mRNA，这是一种鸟苷酸环化酶。NPPC 增加了卵丘细胞和卵母细胞中的 cGMP 水平，并抑制了体外的减数分裂恢复。在 Nppc 或 Npr2 突变小鼠的大多数格拉夫氏卵泡中，减数分裂阻滞不能维持，减数分裂过早恢复。卵母细胞衍生的旁分泌因子促进了卵丘细胞中 Npr2 mRNA 的表达。因此，颗粒细胞配体 NPPC 和其在卵丘细胞中的受体 NPR2 防止了卵母细胞的过早减数分裂成熟，这对于成熟和排卵同步以及正常的雌性生育能力至关重要。
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