Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation
Estrogen is a steroid hormone that plays a key role in regulating many physiological processes, such as follicle activation and development and oocyte maturation in mammals. Ca<sup>2+</sup> is crucial in oogenesis, oocyte maturation, ovulation, and fertilization. However, the mechanism b...
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2024-11-01
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| author | Qingyang Liu Jingmei Li Yanxue Li Ming Cheng Hui Zhang Baohua Ma |
| author_facet | Qingyang Liu Jingmei Li Yanxue Li Ming Cheng Hui Zhang Baohua Ma |
| author_sort | Qingyang Liu |
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| description | Estrogen is a steroid hormone that plays a key role in regulating many physiological processes, such as follicle activation and development and oocyte maturation in mammals. Ca<sup>2+</sup> is crucial in oogenesis, oocyte maturation, ovulation, and fertilization. However, the mechanism by which estrogen regulates Ca<sup>2+</sup> during oocyte maturation in mice has not been reported. This study revealed that Ca<sup>2+</sup> levels in oocytes significantly increase during the 4–12 h period in vitro. Oocytes treated with 0.1 µM estrogen and 1 µM G1, a G-protein-coupled estrogen receptor (GPER) agonist, showed significantly increased Ca<sup>2+</sup> levels, while treatment with 1 µM G15, an antagonist of GPER, significantly decreased Ca<sup>2+</sup> levels. Notably, estrogen regulates Ca<sup>2+</sup> in oocytes through the GPER pathway and promotes the expression of the Ca<sup>2+</sup>-producing protein EPAC1. In addition, estrogen alleviates the inhibitory effect of the Ca<sup>2+</sup> chelator BAPTA-AM during oocyte maturation by promoting Ca<sup>2+</sup> production. Furthermore, estrogen can promote the expression of the mitochondrial generation-associated protein SIRT1 through the GPER pathway, alleviate mitochondrial oxidative damage caused by BAPTA-AM, and restore the mitochondrial membrane potential level. Collectively, this study demonstrates that estrogen can regulate Ca<sup>2+</sup> through the GPER-EPAC1 pathway and promote the expression of SIRT1, which promotes oocyte mitochondrial function during oocyte maturation. |
| format | Article |
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| institution | OA Journals |
| issn | 2218-273X |
| language | English |
| publishDate | 2024-11-01 |
| publisher | MDPI AG |
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| series | Biomolecules |
| spelling | doaj-art-c8fca698c40d46518d8dc9b730f3d32d2025-08-20T02:28:07ZengMDPI AGBiomolecules2218-273X2024-11-011411143010.3390/biom14111430Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte MaturationQingyang Liu0Jingmei Li1Yanxue Li2Ming Cheng3Hui Zhang4Baohua Ma5College of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaEstrogen is a steroid hormone that plays a key role in regulating many physiological processes, such as follicle activation and development and oocyte maturation in mammals. Ca<sup>2+</sup> is crucial in oogenesis, oocyte maturation, ovulation, and fertilization. However, the mechanism by which estrogen regulates Ca<sup>2+</sup> during oocyte maturation in mice has not been reported. This study revealed that Ca<sup>2+</sup> levels in oocytes significantly increase during the 4–12 h period in vitro. Oocytes treated with 0.1 µM estrogen and 1 µM G1, a G-protein-coupled estrogen receptor (GPER) agonist, showed significantly increased Ca<sup>2+</sup> levels, while treatment with 1 µM G15, an antagonist of GPER, significantly decreased Ca<sup>2+</sup> levels. Notably, estrogen regulates Ca<sup>2+</sup> in oocytes through the GPER pathway and promotes the expression of the Ca<sup>2+</sup>-producing protein EPAC1. In addition, estrogen alleviates the inhibitory effect of the Ca<sup>2+</sup> chelator BAPTA-AM during oocyte maturation by promoting Ca<sup>2+</sup> production. Furthermore, estrogen can promote the expression of the mitochondrial generation-associated protein SIRT1 through the GPER pathway, alleviate mitochondrial oxidative damage caused by BAPTA-AM, and restore the mitochondrial membrane potential level. Collectively, this study demonstrates that estrogen can regulate Ca<sup>2+</sup> through the GPER-EPAC1 pathway and promote the expression of SIRT1, which promotes oocyte mitochondrial function during oocyte maturation.https://www.mdpi.com/2218-273X/14/11/1430estrogencalciumoocyte maturationmice |
| spellingShingle | Qingyang Liu Jingmei Li Yanxue Li Ming Cheng Hui Zhang Baohua Ma Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation Biomolecules estrogen calcium oocyte maturation mice |
| title | Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation |
| title_full | Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation |
| title_fullStr | Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation |
| title_full_unstemmed | Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation |
| title_short | Estrogen Regulates Ca<sup>2+</sup> to Promote Mitochondrial Function Through G-Protein-Coupled Estrogen Receptors During Oocyte Maturation |
| title_sort | estrogen regulates ca sup 2 sup to promote mitochondrial function through g protein coupled estrogen receptors during oocyte maturation |
| topic | estrogen calcium oocyte maturation mice |
| url | https://www.mdpi.com/2218-273X/14/11/1430 |
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