Mitochondrial Calcium Disorder Affects Early Embryonic Development in Mice through Regulating the ERK/MAPK Pathway

文献类型： 外文期刊

第一作者： Zhang, Luyao

作者： Zhang, Luyao;Liu, Kexiong;Liu, Zhiqiang;Meng, Lin;Hou, Yunpeng;Zhuan, Qingrui;Fu, Xiangwei;Fu, Xiangwei;Jia, Gongxue;Jia, Gongxue

作者机构：

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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