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卵巢颗粒细胞中的上皮钠离子通道 (ENaC) 调节钙动员和促性腺激素信号转导，以维持雌激素平衡和女性生育能力。

The epithelial Na channel (ENaC) in ovarian granulosa cells modulates Ca mobilization and gonadotrophin signaling for estrogen homeostasis and female fertility.

机构信息

Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong SAR, China.

Jinan University, Guangzhou, China.

出版信息

Cell Commun Signal. 2024 Aug 14;22(1):398. doi: 10.1186/s12964-024-01778-5.

DOI:10.1186/s12964-024-01778-5
PMID:39143495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11323461/
Abstract

Ovarian granulosa cells are essential to gonadotrophin-regulated estrogen production, female cycle maintenance and fertility. The epithelial Na channel (ENaC) is associated with female fertility; however, whether and how it plays a role in ovarian cell function(s) remained unexplored. Here, we report patch-clamp and Na imaging detection of ENaC expression and channel activity in both human and mouse ovarian granulosa cells, which are promoted by pituitary gonadotrophins, follicle stimulating hormone (FSH) or luteinizing hormone (LH). Cre-recombinase- and CRISPR-Cas9-based granulosa-specific knockout of ENaC α subunit (Scnn1a) in mice resulted in failed estrogen elevation at early estrus, reduced number of corpus luteum, abnormally extended estrus phase, reduced litter size and subfertility in adult female mice. Further analysis using technologies including RNA sequencing and Ca imaging revealed that pharmacological inhibition, shRNA-based knockdown or the knockout of ENaC diminished spontaneous or stimulated Ca oscillations, lowered the capacity of intracellular Ca stores and impaired FSH/LH-stimulated transcriptome changes for estrogen production in mouse and/or human granulosa cells. Together, these results have revealed a previously undefined role of ENaC in modulating gonadotrophin signaling in granulosa cells for estrogen homeostasis and thus female fertility.

摘要

卵巢颗粒细胞对于促性腺激素调节的雌激素产生、女性周期维持和生育能力至关重要。上皮钠通道 (ENaC) 与女性生育力有关；然而，它是否以及如何在卵巢细胞功能中发挥作用仍未被探索。在这里，我们报告了在人和小鼠的卵巢颗粒细胞中检测到 ENaC 表达和通道活性的膜片钳和 Na 成像，这些细胞受到垂体促性腺激素、卵泡刺激素 (FSH) 或黄体生成素 (LH) 的促进。在小鼠中使用 Cre 重组酶和 CRISPR-Cas9 进行颗粒细胞特异性 ENaCα亚基 (Scnn1a) 基因敲除导致早期发情时雌激素升高失败、黄体数量减少、发情期异常延长、幼仔数量减少和成年雌性小鼠的生育能力下降。使用包括 RNA 测序和 Ca 成像在内的技术进行的进一步分析表明，ENaC 的药理学抑制、shRNA 敲低或基因敲除减弱了自发或刺激的 Ca 振荡，降低了细胞内 Ca 储存的能力，并损害了 FSH/LH 刺激的转录组变化，从而减少了小鼠和/或人颗粒细胞中雌激素的产生。总之，这些结果揭示了 ENaC 在调节颗粒细胞中促性腺激素信号以维持雌激素平衡和女性生育能力方面的先前未定义的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/1e9360415e7e/12964_2024_1778_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/96f715835203/12964_2024_1778_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/bbc84d73b5fe/12964_2024_1778_Fig6_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/b2b6d5f50824/12964_2024_1778_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/1e9360415e7e/12964_2024_1778_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/2cac24c81b65/12964_2024_1778_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/f5cfba7c7fbc/12964_2024_1778_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/affd0dfa1ec6/12964_2024_1778_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/5a6b4e0346fc/12964_2024_1778_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/96f715835203/12964_2024_1778_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/bbc84d73b5fe/12964_2024_1778_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/32439bbf4d5e/12964_2024_1778_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/b2b6d5f50824/12964_2024_1778_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee33/11323461/1e9360415e7e/12964_2024_1778_Fig9_HTML.jpg

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