Effects of mitochondria‐associated Ca2+ transporters suppression on oocyte activation. (8th July 2020)

• Record Type: Journal Article
• Authors: Wang, Feng; Li, Ang; Li, Qian‐Nan; Fan, Li‐Hua; Wang, Zhen‐Bo; Meng, Tie‐Gang; Hou, Yi; Schatten, Heide; Sun, Qing‐Yuan; Ou, Xiang‐Hong
• Is Part Of: Cell biochemistry and function. Volume 39:Number 2(2021)
• Page Start: 248
• Page End: 257
• Publication Date: 2020-07-08
• Subjects: mitochondria -- mitochondrial Ca2+ transport -- mitochondrial membrane potential -- oocyte activation; Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3571
• Languages: English
• ISSNs: 0263-6484

Abstract

Abstract : 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.