Mitochondrial Calcium Disorder Affects Early Embryonic Development in Mice through Regulating the ERK/MAPK Pathway
文献类型： 外文期刊
作者： Zhang, Luyao 1 ; Liu, Kexiong 1 ; Zhuan, Qingrui 2 ; Liu, Zhiqiang 1 ; Meng, Lin 1 ; Fu, Xiangwei 2 ; Jia, Gongxue 4 ; Hou, Yunpeng 1 ;
作者机构： 1.China Agr Univ, Coll Biol Sci, State Key Labs Agrobiotechnol, Beijing, Peoples R China
2.China Agr Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding & Reprod, Beijing, Peoples R China
3.Xinjiang Acad Agr & Reclamat Sci, State Key Lab Sheep Genet Improvement & Hlth Breed, Shihezi, Peoples R China
4.Chinese Acad Sci, Northwest Inst Plateau Biol, Key Lab Adaptat & Evolut Plateau Biota, Xining, Qinghai, Peoples R China
5.Chinese Acad Sci, Northwest Inst Plateau Biol, Qinghai Prov Key Lab Anim Ecol Genom, Xining, Qinghai, Peoples R China
期刊名称：OXIDATIVE MEDICINE AND CELLULAR LONGEVITY （ 影响因子：7.31； 五年影响因子：8.427 ）
ISSN： 1942-0900
年卷期： 2022 年 2022 卷
页码：
收录情况： SCI
摘要： The homeostasis of mitochondrial calcium ([Ca2+](mt)) in oocytes plays a critical role in maintaining normal reproductive cellular progress such as meiosis. However, little is known about the association between [Ca2+](mt) homeostasis and early embryonic development. Two in vitro mouse MII oocyte models were established by using a specific agonist or inhibitor targeting mitochondrial calcium uniporters (MCU) to upregulate or downregulate [Ca2+](mt) concentrations. The imbalance of [Ca2+](mt) in MII oocytes causes mitochondrial dysfunction and morphological abnormity, leading to an abnormal spindle/chromosome structure. Oocytes in drug-treated groups are less likely to develop into blastocyst during in vitro culture. Abnormal [Ca2+](mt) concentrations in oocytes hindered epigenetic modification and regulated mitogen-activated protein kinase (MAPK) signaling that is associated with gene expression. We also found that MAPK/ERK signaling is regulating DNA methylation in MII oocytes to modulate epigenetic modification. These data provide a new insight into the protective role of [Ca2+](mt) homeostasis in early embryonic development and also demonstrate a new mechanism of MAPK signaling regulated by [Ca2+](mt) that influences epigenetic modification.
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