论文成果
Involvement of MEK-mitogen-activated protein kinase pathway in follicle-stimulating hormone-induced but not spontaneous meiotic resumption of mouse oocytes
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发表刊物：
Biology of Reproduction
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刊物所在地：
USA
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关键字：
developmental biology, FSH, kinases, meiosis, oocyte development, ovum, signal transduction
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摘要：
Mitogen-activated protein (MAP) kinase has been reported to be activated during oocyte meiotic maturation in a variety of mammalian species. However, the mechanism(s) responsible for MAP kinase activation and the consequence of its premature activation during gonadotropin-induced oocyte meiotic resumption have not been examined. The present experiments were conducted to investigate the possible role of MAP kinase in FSH-induced and spontaneous oocyte meiotic resumption in the mouse. MAP kinase kinase (MAPKK, MEK) inhibitor, PD98059 or U0126, produced a dose-dependent inhibitory effect on both FSH-induced oocyte meiotic resumption and MAP kinase activation in the oocytes. However, the same inhibitor did not block spontaneous meiotic resumption of either denuded or cumulus cell-enclosed mouse oocytes, despite the activity of MAP kinase being totally inhibited. Immunoblotting the oocytes and the cumulus cells with the anti-active MAP kinase antibody showed that MAP kinase activity in the oocytes was detected at 8 h of FSH treatment, prior to germinal vesicle breakdown and increased as maturation progressed in the following culture period. In the cumulus cells, MAP kinase was activated even faster, its activity was detected at 1 h of FSH stimulation and increased gradually until 8 h of FSH treatment, then decreased and diminished after 12 h of FSH action. These data demonstrated that the MEK-MAP kinase pathway is implicated in FSH-induced but not spontaneous oocyte meiotic resumption.
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全部作者：
S Rubinstein, A Luria, Y Lax
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第一作者：
You-Qiang Su
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论文类型：
RESEARCH ARTICLE
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通讯作者：
H Breitbart
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论文编号：
10.1095/biolreprod65.2.358
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卷号：
65
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期号：
2
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页面范围：
358-365
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ISSN号：
0006-3363
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是否译文：
否
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发表时间：
2001-08-01
上一条：Mitogen-activated protein kinase activity in cumulus cells is essential for gonadotropin-induced oocyte meiotic resumption and cumulus expansion in the mouse
下一条：Pathogenic variants of TUBB8 cause oocyte spindle defects by disrupting with EB1-CAKP5 interactions and potential treatment targeting microtubule acetylation through HDAC6 inhibition.
