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首页> 外文期刊>Endocrinology >Subfertile female androgen receptor knockout mice exhibit defects in neuroendocrine signaling, intraovarian function, and uterine development but not uterine function.
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Subfertile female androgen receptor knockout mice exhibit defects in neuroendocrine signaling, intraovarian function, and uterine development but not uterine function.

机译：雌性雄性激素受体敲除小鼠在神经内分泌信号传导，卵巢内功能和子宫发育方面表现出缺陷，但在子宫功能中却没有。

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Female androgen receptor (AR) knockout mice (AR(-/-)) generated by an in-frame Ar exon 3 deletion are subfertile, but the mechanism is not clearly defined. To distinguish between extra- and intraovarian defects, reciprocal ovarian transplants were undertaken. Ovariectomized AR(-/-) hosts with wild-type (AR(+/+)) ovary transplants displayed abnormal estrus cycles, with longer cycles (50%, P < 0.05), and 66% were infertile (P < 0.05), whereas AR(+/+) hosts with either AR(-/-) or surgical control AR(+/+) ovary transplants displayed normal estrus cycles and fertility. These data imply a neuroendocrine defect, which is further supported by increased FSH (P <0.05) and estradiol (P <0.05), and greater LH suppressibility by estradiol in AR(-/-) females at estrus (P <0.05). Additional intraovarian defects were observed by the finding that both experimental transplant groups exhibited significantly reduced pups per litter (P < 0.05) and corpora lutea numbers (P < 0.05) compared with surgical controls. All groups exhibited normal uterine and lactation functions. AR(-/-) uteri were morphologically different from AR(+/+) with an increase in horn length (P < 0.01) but a reduction in uterine diameter (P < 0.05), total uterine area (P < 0.05), endometrial area (P < 0.05), and myometrial area (P < 0.01) at diestrus, indicating a role for AR in uterine growth and development. Both experimental transplant groups displayed a significant reduction in uterine diameter (P < 0.01) compared with transplanted wild-type controls, indicating a role for both AR-mediated intraovarian and intrauterine influences on uterine physiology. In conclusion, these data provide direct evidence that extraovarian neuroendocrine, but not uterine effects, as well as local intraovarian AR-mediated actions are important in maintaining female fertility, and a disruption of AR signaling leads to altered uterine development.
机译：框内Ar外显子3缺失产生的雌性雄激素受体（AR）基因敲除小鼠（AR（-/-））较不育，但机制尚不清楚。为了区分卵巢外缺陷和卵巢内缺陷，进行了相互卵巢移植。卵巢切除的具有野生型（AR（+ / +））卵巢移植的AR（-/-）宿主表现出异常的发情周期，周期较长（50％，P <0.05），不育的占66％（P <0.05），而具有AR（-/-）或手术控制的AR（+ / +）宿主或AR（+ / +）卵巢移植宿主表现出正常的发情周期和生育能力。这些数据表明存在神经内分泌缺陷，进一步由FSH（P <0.05）和雌二醇（P <0.05）增加，并且雌二醇在发情期AR（-/-）雌性中对LH的抑制作用更大（P <0.05）。通过发现与手术对照组相比，两个实验移植组的每窝幼仔数（P <0.05）和黄体数（P <0.05）均发现了其他卵巢内缺陷。所有组均表现出正常的子宫和泌乳功能。 AR（-/-）子宫在形态学上与AR（+ / +）不同，其角长增加（P <0.01），但子宫直径减小（P <0.05），子宫总面积（P <0.05），子宫内膜面积（P <0.05）和子宫肌层面积（P <0.01）位于二头肌，表明AR在子宫生长发育中起一定作用。与移植的野生型对照相比，两个实验移植组均显示子宫直径显着减小（P <0.01），表明AR介导的卵巢内和子宫内对子宫生理的影响均起作用。总之，这些数据提供了直接的证据，即卵巢外神经内分泌而非子宫作用以及局部卵巢内AR介导的作用在维持女性生育力中很重要，AR信号的破坏导致子宫发育改变。

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