雄激素在卵泡成熟和闭锁中的作用

PhD, DSc, FRCPath Stephen G. Hillier (Professor of Reproductive Endocrinology), PhD Masa Tetsuka (Medical Research Council Research Fellow)
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引用次数: 182

摘要

雄激素是孕激素代谢的产物,雌激素生物合成的中间体和卵巢功能的局部调节剂。综述了目前对卵巢内雄激素形成、代谢和作用的认识,重点介绍了雄激素在卵泡成熟和闭锁的旁分泌调节中的作用。任何改变细胞内cAMP水平的因素都是颗粒细胞分化和卵泡发育的潜在调节剂。雄激素似乎通过放大camp介导的受体后信号传导来调节促性腺激素对颗粒细胞的作用。本文认为,在卵泡发育的中间阶段,局部产生的雄激素通过颗粒细胞雄激素受体(AR)通过放大camp介导的受体后信号传导,促进促卵泡激素(FSH)诱导的颗粒细胞分化。在排卵前卵泡发育后期,黄体生成素(LH)刺激引起的高浓度cAMP抑制颗粒细胞增殖,并下调FSH在排卵前发育早期诱导的一些基因,包括芳香酶活性。其他颗粒细胞功能,包括黄体酮合成,可通过LH诱导的高浓度cAMP增强。在对大鼠和非人类灵长类动物(普通狨猴)卵巢的研究中,有实验证据表明,颗粒细胞中的AR水平在排卵前卵泡成熟期间下降。由于雄激素增强了fsh诱导的cAMP形成和作用,AR的丧失可能是避免不适当的高cAMP水平的一种手段,从而避免过早激活导致闭锁的“高音调”cAMP反应基因。颗粒细胞AR的负调控可能是卵巢内机制的一部分,该机制决定了在正常月经周期中哪个卵泡占主导地位并分泌雌激素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
3 Role of androgens in follicle maturation and atresia

Androgens are products of progestogen metabolism, intermediates in oestrogen biosynthesis and local regulators of ovarian function. Current understanding of intraovarian androgen formation, metabolism and action is reviewed, highlighting the contribution of androgens to the paracrine regulation of follicular maturation and atresia. Any factor that alters intracellular cAMP levels is a potential modulator of granulosa cell differentiation, and hence follicular development. Androgen appears to modulate gonadotrophin action on granulosa cells through amplification of cAMP-mediated post-receptor signalling. Here it is argued that during intermediate stages of follicular development, locally produced androgen acts via granulosa cell androgen receptors (AR) to promote follicle-stimulating hormone (FSH)-induced granulosa cell differentiation through amplifying cAMP-mediated post-receptor signalling. During late pre-ovulatory follicular development, higher concentrations of cAMP caused by stimulation with luteinizing hormone (LH) suppress granulosa cell proliferation and down-regulate some of the genes induced by FSH at earlier stages of pre-ovulatory development, including aromatase activity. Other granulosa cell functions, including progesterone synthesis, are enhanced by the high concentrations of cAMP induced by LH. There is experimental evidence from studies of rat and non-human primate (common marmoset) ovaries that AR levels in granulosa cells decline during pre-ovulatory follicular maturation. Since androgens augment FSH-induced cAMP formation and action, loss of AR could be a means of avoiding inappropriately high cAMP levels and hence avoiding premature activation of ‘high-tone’ cAMP-response genes that lead to atresia. Negative regulation of the granulosa cell AR could be part of the intra-ovarian mechanism that determines which follicle(s) becomes dominant and secretes oestrogen in the normal menstrual cycle.

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