哺乳动物减数分裂恢复过程中丝裂原活化蛋白激酶3/1活性的调控

R. Procházka, M. Blaha
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引用次数: 21

摘要

在体内,黄体生成素(LH)在排卵前激增后,大卵泡中发生卵母细胞减数分裂的恢复。黄体生成素激增导致配备有黄体生成素受体的壁粒细胞中广泛信号网络的激活。壁粒细胞产生的信号被局部产生的肽或类固醇进一步增强,并转移到卵丘细胞室和卵母细胞本身。在过去的十年中,在确定与哺乳动物卵母细胞最终成熟和排卵相关的分子事件方面取得了重要进展。所有新的证据都表明,丝裂原活化蛋白激酶3/1 (MAPK3/1)在促性腺激素诱导的排卵过程中起着多种作用。然而,对促性腺激素诱导的导致滤泡细胞中MAPK3/1激活的信号通路的了解似乎有限。迄今为止,尽管在其他类型的细胞中已经检测到MAPK3/1激活的其他机制,但在颗粒/云细胞中仅描述了lh诱导的表皮生长因子受体/MAPK3/1途径的转激活。在这篇综述中,我们旨在总结促性腺激素诱导的MAPK3/1在排卵前卵泡和培养的卵丘-卵母细胞复合物中激活的机制的最新进展,并指出该激酶在哺乳动物卵母细胞最终成熟过程中的特定作用。
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Regulation of mitogen-activated protein kinase 3/1 activity during meiosis resumption in mammals
In vivo, resumption of oocyte meiosis occurs in large ovarian follicles after the preovulatory surge of luteinizing hormone (LH). The LH surge leads to the activation of a broad signaling network in mural granulosa cells equipped with LH receptors. The signals generated in the mural granulosa cells are further augmented by locally produced peptides or steroids and transferred to the cumulus cell compartment and the oocyte itself. Over the last decade, essential progress has been made in the identification of molecular events associated with the final maturation and ovulation of mammalian oocytes. All new evidence argues for a multiple roles of mitogen-activated protein kinase 3/1 (MAPK3/1) in the gonadotropin-induced ovulation processes. However, the knowledge of gonadotropin-induced signaling pathways leading to MAPK3/1 activation in follicular cells seems limited. To date, only the LH-induced transactivation of the epidermal growth factor receptor/MAPK3/1 pathway has been described in granulosa/cumulus cells even though other mechanisms of MAPK3/1 activation have been detected in other types of cells. In this review, we aimed to summarize recent advances in the elucidation of gonadotropin-induced mechanisms leading to the activation of MAPK3/1 in preovulatory follicles and cultured cumulus-oocyte complexes and to point out a specific role of this kinase in the processes accompanying final maturation of the mammalian oocyte.
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