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孕激素受体膜成分 1 介导孕激素诱导的卵母细胞减数分裂前期 I 和原始卵泡发生的抑制作用。

Progesterone Receptor Membrane Component 1 Mediates Progesterone-Induced Suppression of Oocyte Meiotic Prophase I and Primordial Folliculogenesis.

机构信息

Department of Laboratory Animal Science, School of Basic Medical Science, Capital Medical University, Beijing 100069, Peoples' Republic of China.

College of Life Science, Capital Normal University, Beijing 100048, People's Republic of China.

出版信息

Sci Rep. 2016 Nov 16;6:36869. doi: 10.1038/srep36869.

DOI:10.1038/srep36869
PMID:27848973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5111101/
Abstract

Well-timed progression of primordial folliculogenesis is essential for mammalian female fertility. Progesterone (P4) inhibits primordial follicle formation under physiological conditions; however, P4 receptor that mediates this effect and its underlying mechanisms are unclear. In this study, we used an in vitro organ culture system to show that progesterone receptor membrane component 1 (PGRMC1) mediated P4-induced inhibition of oocyte meiotic prophase I and primordial follicle formation. We found that membrane-impermeable BSA-conjugated P4 inhibited primordial follicle formation similar to that by P4. Interestingly, PGRMC1 and its partner serpine1 mRNA-binding protein 1 were highly expressed in oocytes in perinatal ovaries. Inhibition or RNA interference of PGRMC1 abolished the suppressive effect of P4 on follicle formation. Furthermore, P4-PGRMC1 interaction blocked oocyte meiotic progression and decreased intra-oocyte cyclic AMP (cAMP) levels in perinatal ovaries. cAMP analog dibutyryl cAMP reversed P4-PGRMC1 interaction-induced inhibition of meiotic progression and follicle formation. Thus, our results indicated that PGRMC1 mediated P4-induced suppression of oocyte meiotic progression and primordial folliculogenesis by decreasing intra-oocyte cAMP levels.

摘要

原始卵泡发生的适时进展对于哺乳动物雌性生育能力至关重要。孕激素（P4）在生理条件下抑制原始卵泡的形成；然而，介导这种效应及其潜在机制的孕激素受体尚不清楚。在这项研究中，我们使用体外器官培养系统表明，孕激素受体膜成分 1（PGRMC1）介导了 P4 诱导的减数分裂前期 I 和原始卵泡形成的抑制作用。我们发现，膜不可渗透的 BSA 缀合 P4 抑制原始卵泡形成的作用类似于 P4。有趣的是，PGRMC1 及其伴侣丝氨酸蛋白酶抑制剂 1 mRNA 结合蛋白 1 在围产期卵巢中的卵母细胞中高表达。PGRMC1 的抑制或 RNA 干扰消除了 P4 对卵泡形成的抑制作用。此外，P4-PGRMC1 相互作用阻断了卵母细胞减数分裂进程，并降低了围产期卵巢中的卵内环磷酸腺苷（cAMP）水平。cAMP 类似物二丁酰基 cAMP 逆转了 P4-PGRMC1 相互作用诱导的减数分裂进程和卵泡形成抑制。因此，我们的研究结果表明，PGRMC1 通过降低卵内 cAMP 水平介导了 P4 诱导的卵母细胞减数分裂进程和原始卵泡发生的抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/4d51a8865d39/srep36869-f8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/eb89948c3fd4/srep36869-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/e528eaceda01/srep36869-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/4d51a8865d39/srep36869-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/16288e0913cc/srep36869-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/c721c602b967/srep36869-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/f6b3285c16c7/srep36869-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/7c54922d0cee/srep36869-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/f8ea3fb35418/srep36869-f5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/e528eaceda01/srep36869-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a58d/5111101/4d51a8865d39/srep36869-f8.jpg

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