MAPK3/1 (ERK1/2) in ovarian granulosa cells are essential for female fertility.
MAPK3/1 (ERK1/2) in ovarian granulosa cells are essential for female fertility.
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DOI：
10.1126/science.1171396
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发表时间：
2009-05-15
期刊：
影响因子：
--
通讯作者：
Richards JS
中科院分区：
文献类型：
--
作者：
Fan HY;Liu Z;Shimada M;Sterneck E;Johnson PF;Hedrick SM;Richards JS
垂体分泌的促黄体生成激素（LH）能触发哺乳动物排卵、卵母细胞成熟和黄体化，从而促进哺乳动物的成功繁殖。由于信号分子RAS和ERK 1/2（细胞外信号调节激酶1和2）被激活的LH峰在排卵前卵泡的颗粒细胞，我们破坏Erk 1/2在小鼠颗粒细胞，并提供在体内的证据表明，这些激酶是LH诱导的卵母细胞减数分裂，排卵和黄体化的恢复所必需的。此外，颗粒细胞中Cebpb基因的生化分析和选择性破坏表明C/EBPβ（CCAAT/增强子结合蛋白-β）是ERK 1/2激活的关键下游介质。因此，ERK 1/2和C/EBPβ构成体内LH调节的信号通路，控制排卵和黄体化相关事件。
A surge of luteinizing hormone (LH) from the pituitary gland triggers ovulation, oocyte maturation, and luteinization for successful reproduction in mammals. Because the signaling molecules RAS and ERK1/2 (extracellular signal–regulated kinases 1 and 2) are activated by an LH surge in granulosa cells of preovulatory follicles, we disrupted Erk1/2 in mouse granulosa cells and provide in vivo evidence that these kinases are necessary for LH-induced oocyte resumption of meiosis, ovulation, and luteinization. In addition, biochemical analyses and selected disruption of the Cebpb gene in granulosa cells demonstrate that C/EBPβ (CCAAT/Enhancer-binding protein–β) is a critical downstream mediator of ERK1/2 activation. Thus, ERK1/2 and C/EBPβ constitute an in vivo LH-regulated signaling pathway that controls ovulation- and luteinization-related events.
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