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Effects of m itochondria‐associated Ca 2+ transporters suppression on oocyte activation
Author(s) -
Wang Feng,
Li Ang,
Li QianNan,
Fan LiHua,
Wang ZhenBo,
Meng TieGang,
Hou Yi,
Schatten Heide,
Sun QingYuan,
Ou XiangHong
Publication year - 2021
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3571
Subject(s) - uniporter , oocyte , mitochondrion , microbiology and biotechnology , oocyte activation , voltage dependent anion channel , chemistry , calcium , biophysics , cytosol , biology , biochemistry , embryo , organic chemistry , escherichia coli , bacterial outer membrane , gene , enzyme
Oocyte activation deficiency leads to female infertility. [Ca 2+ ] i oscillations are required for mitochondrial energy supplement transition from the resting to the excited state, but the underlying mechanisms are still very little known. Three mitochondrial Ca 2+ channels, Mitochondria Calcium Uniporter (MCU), Na + /Ca 2+ Exchanger (NCLX) and Voltage‐dependent Ca 2+ Channel (VDAC), were deactivated by inhibitors RU360, CGP37157 and Erastin, respectively. Both Erastin and CGP37157 inhibited mitochondrial activity significantly while attenuating [Ca 2+ ] i and [Ca 2+ ] m oscillations, which caused developmental block of pronuclear formation. Thus, NCLX and VDAC are two mitochondria‐associated Ca 2+ transporter proteins regulating oocyte activation, which may be used as potential targets to treat female infertility. Significance of the Study NCLX and VDAC are two mitochondria‐associated Ca 2+ transporter proteins regulating oocyte activation.