Effects of mitochondria-associated Ca2+ transporters suppression on oocyte activation

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. SIGNIFICANCE OF THE STUDY: NCLX and VDAC are two mitochondria-associated Ca²⁺ transporter proteins regulating oocyte activation.

Keywords: mitochondria; mitochondrial Ca2+ transport; mitochondrial membrane potential; oocyte activation.