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内皮素-1对卵母细胞减数分裂恢复的旁分泌调节。

Paracrine regulation of the resumption of oocyte meiosis by endothelin-1.

作者信息

Kawamura Kazuhiro, Ye Yinghui, Liang Cheng Guang, Kawamura Nanami, Gelpke Maarten Sollewijn, Rauch Rami, Tanaka Toshinobu, Hsueh Aaron J W

机构信息

Department of Obstetrics and Gynecology, Akita University School of Medicine, Akita 010-8543, Japan.

出版信息

Dev Biol. 2009 Mar 1;327(1):62-70. doi: 10.1016/j.ydbio.2008.11.033. Epub 2008 Dec 7.

Abstract

Mammalian oocytes remain dormant in the diplotene stage of prophase I until the resumption of meiosis characterized by germinal vesicle breakdown (GVBD) following the preovulatory gonadotropin stimulation. Based on genome-wide analysis of peri-ovulatory DNA microarray to identify paracrine hormone-receptor pairs, we found increases in ovarian transcripts for endothelin-1 and endothelin receptor type A (EDNRA) in response to the preovulatory luteinizing hormone (LH)/human chorionic gonadotropin (hCG) stimulation. Immunohistochemical analyses demonstrated localization of EDNRA in granulosa and cumulus cells. In cultured preovulatory follicles, treatment with endothelin-1 promoted oocyte GVBD. The stimulatory effect of endothelin-1 was blocked by cotreatment with antagonists for the type A, but not related type B, receptor. The stimulatory effect of hCG on GVBD was partially blocked by the same antagonist. The endothelin-1 promotion of GVBD was found to be mediated by the MAPK/ERK pathway but not by the inhibitory G protein. Studies using cumulus-oocyte complexes and denuded oocytes demonstrated that the endothelin-1 actions are mediated by cumulus cells. Furthermore, intrabursal administration with endothelin-1 induced oocyte GVBD in preovulatory follicles. Our findings demonstrate a paracrine role of endothelin-1 in the induction of the resumption of meiosis and provide further understanding on the molecular mechanisms underlying the nuclear maturation of oocytes induced by the preovulatory LH surge.

摘要

哺乳动物卵母细胞在减数分裂前期I的双线期处于休眠状态,直到排卵前促性腺激素刺激后,以生发泡破裂(GVBD)为特征的减数分裂恢复。基于对排卵周围DNA微阵列的全基因组分析以鉴定旁分泌激素-受体对,我们发现,响应排卵前促黄体生成素(LH)/人绒毛膜促性腺激素(hCG)刺激,卵巢中内皮素-1和A型内皮素受体(EDNRA)的转录物增加。免疫组织化学分析表明EDNRA定位于颗粒细胞和卵丘细胞中。在培养的排卵前卵泡中,用内皮素-1处理可促进卵母细胞GVBD。内皮素-1的刺激作用被A型受体拮抗剂共处理所阻断,但不被相关的B型受体拮抗剂阻断。hCG对GVBD的刺激作用被相同的拮抗剂部分阻断。发现内皮素-1促进GVBD是由MAPK/ERK途径介导的,而不是由抑制性G蛋白介导的。使用卵丘-卵母细胞复合体和裸卵进行的研究表明,内皮素-1的作用是由卵丘细胞介导的。此外,向卵泡腔内注射内皮素-1可诱导排卵前卵泡中的卵母细胞GVBD。我们的研究结果证明了内皮素-1在诱导减数分裂恢复中的旁分泌作用,并为排卵前LH峰诱导卵母细胞核成熟的分子机制提供了进一步的理解。

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