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Oocyte activation deficiency leads to female infertility. [Ca2+]i oscillations are required for mitochondrial energy supplement transition from the resting to the excited state, but the underlying mechanisms are still very… Click to show full abstract
Oocyte activation deficiency leads to female infertility. [Ca2+]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 Ca2+ channels, Mitochondria Calcium Uniporter (MCU), Na+/Ca2+ Exchanger (NCLX) and Voltage‐dependent Ca2+ Channel (VDAC), were deactivated by inhibitors RU360, CGP37157 and Erastin, respectively. Both Erastin and CGP37157 inhibited mitochondrial activity significantly while attenuating [Ca2+]i and [Ca2+]m oscillations, which caused developmental block of pronuclear formation. Thus, NCLX and VDAC are two mitochondria‐associated Ca2+ transporter proteins regulating oocyte activation, which may be used as potential targets to treat female infertility.
Journal Title: Cell Biochemistry and Function
Year Published: 2020
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