Are steroids obligatory mediators of Luteinizing Hormone/human chorionic gonadotropin-triggered resumption of meiosis in mammals?
Are steroids obligatory mediators of Luteinizing Hormone/human chorionic gonadotropin-triggered resumption of meiosis in mammals?
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DOI：
10.1210/en.2007-0445
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发表时间：
2007-09-01
期刊：
影响因子：
4.8
通讯作者：
Tsafriri, Alex
中科院分区：
文献类型：
--
作者：
Motola, Shmulik;Popliker, Malka;Tsafriri, Alex
类固醇介导鱼类和两栖类卵母细胞成熟的促性腺刺激。类固醇在哺乳动物中的这种作用直到最近才得到证实。一系列的研究表明，类固醇激素可能参与小鼠卵母细胞减数分裂。在这里，我们研究了这一建议，在体外培养的大鼠和小鼠卵泡封闭的卵母细胞（FEOs）和卵丘封闭的卵母细胞（CEOs）。在仅对促性腺激素或其他刺激物有反应的FEO中，我们测试了类固醇触发减数分裂的能力，以及类固醇受体拮抗剂的加入是否阻断LH/人绒毛膜促性腺激素刺激减数分裂。在自发成熟的CEO中，我们测试了类固醇拮抗剂是否阻断成熟，以及类固醇是否克服了次黄嘌呤（Hx）对成熟的抑制，次黄嘌呤是一种温和的减数分裂恢复抑制剂。孕酮拮抗剂米非司酮（RU 486）和Organon 31710以及雌激素拮抗剂法仕得（faslodex）不能阻止LH触发的大鼠或小鼠FEOs成熟或CEOs的自发成熟。与此一致，孕酮激动剂普罗美孕酮（R5020）和雌二醇没有刺激大鼠和小鼠FEO减数分裂的恢复，并且都没有克服大鼠和小鼠CEOs减数分裂的Hx抑制。雄激素拮抗剂氟替卡松确实阻断大鼠FEO的减数分裂，但这种作用不受添加双氢睾酮的影响，表明它不是雄激素受体介导的。氟替卡松不影响大鼠CEOs的自发成熟，双氢睾酮不能刺激Hx抑制的减数分裂。因此，与低等脊椎动物相反，在哺乳动物中，类固醇似乎并不作为卵泡体细胞将促性腺激素刺激的减数分裂传递给卵母细胞的强制性信号。
Steroids mediate the gonadotropic stimulus of oocyte maturation in fish and amphibians. Such a role of steroids in mammals has not been confirmed until recently. A series of studies presented data suggesting that steroids might be involved in meiosis of mouse oocytes. Here we examined this suggestion using in vitro cultures of rat and mouse follicle-enclosed oocytes (FEOs) and cumulus-enclosed oocytes (CEOs). In FEOs that mature only in response to gonadotropins or other stimuli, we tested the ability of steroids to trigger meiosis and whether addition of steroid receptor antagonists blocks LH/ human chorionic gonadotropin stimulation of meiosis. In CEOs that mature spontaneously, we tested whether steroid antagonists block maturation and whether steroids overcome the inhibition of maturation by hypoxanthine (Hx), a mild inhibitor of meiotic resumption. The progesterone antagonists mifepristone (RU 486) and Organon 31710 as well as the estrogen antagonist faslodex did not prevent LH-triggered maturation of rat or mouse FEOs or the spontaneous maturation of CEOs. In accordance, the progesterone agonist promegestone ( R5020)and estradiol did not stimulate the resumption of meiosis in rat and mouse FEOs, and both did not overcome the Hx inhibition of meiosis in rat and mouse CEOs. Flutamide, an androgen antagonist, did block meiosis in rat FEOs, but this action could not be affected by adding dihydrotestosterone, suggesting that it was not androgen receptor mediated. Flutamide did not affect spontaneous maturation of rat CEOs, and dihydrotestosterone could not stimulate meiosis inhibited by Hx. Thus, in contrast to lower vertebrates, in mammals, steroids do not seem to serve as an obligatory signal by which the somatic cells of the follicle transfer the gonadotropic stimulation of meiosis to the oocyte.