雌激素调节Ca2+以通过G蛋白合雌激素受体在卵细胞成熟期间促进线粒体功能
Qingyang Liu1,2, Jingmei Li1,2, Yanxue Li1,2
1College of Veterinary Medicine, Northwest A&F University, Yangling 712100, China.
Biomolecules
|November 27, 2024
概括
雌激素通过G蛋白结合雌激素受体 (GPER) 途径调节小鼠卵细胞中的 (Ca2+) 水平,促进卵细胞成熟和线粒体功能.
科学领域:
- 生殖生物学 生殖生物学
- 细胞生理学 细胞生理学
- 内分泌学 在内分泌学.
背景情况:
- 雌激素是哺乳动物繁殖的关键类固醇激素,影响卵细胞成熟.
- (Ca2+) 离子对于产卵,成熟,排卵和受精至关重要.
- 在卵细胞成熟期间雌激素对Ca2+的调节的确切机制尚不清楚.
研究的目的:
- 为了阐明雌激素如何调节小鼠卵细胞成熟期间的细胞内Ca2+水平.
- 研究G蛋白结合雌激素受体 (GPER) 途径在雌激素介导的Ca2+调节中的作用.
- 为了确定雌激素在卵细胞成熟期间对线粒体功能的影响.
主要方法:
- 在实验室培养小鼠卵细胞.
- 在雌激素和GPER特异性激动剂/对抗剂治疗后测量细胞内Ca2+水平.
- 对EPAC1和SIRT1基因表达的分析.
- 评估线粒体功能和氧化损伤.
主要成果:
- 细胞内Ca2+水平在体外成熟期间在卵细胞中显著增加.
- 雌激素和GPER激动剂 (G1) 提高了Ca2+水平,而GPER抗剂 (G15) 降低了它们.
- 雌激素通过GPER上调EPAC1的表达,增强Ca2+的产生,减轻BAPTA-AM的抑制作用.
- 雌激素促进SIRT1的表达,保护线粒体免受氧化损伤,恢复膜潜力.
结论:
- 雌激素通过GPER-EPAC1信号通路调节卵细胞中的Ca2+.
- 雌激素通过促进Ca2+的产生和通过SIRT1.1.支持线粒体功能来增强卵细胞成熟.
- 这项研究揭示了雌激素在哺乳动物卵细胞发育中的新型机制.
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