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Updated: Dec 15, 2025
Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
Published on: April 27, 2018
Effects of mitochondria-associated Ca2+ transporters suppression on oocyte activation
Feng Wang1,2, Ang Li1, Qian-Nan Li1,2
1State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
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.
Insights
Sodium/Calcium Exchanger (NCLX) and Voltage-dependent Calcium Channel (VDAC) regulate oocyte activation. These calcium transporters are crucial for mitochondrial function and female fertility, offering potential therapeutic targets.
Area of Science:
- Reproductive Biology
- Cellular Physiology
- Mitochondrial Function
Background:
- Oocyte activation deficiency causes female infertility.
- Intracellular calcium ([Ca2+]i) oscillations are vital for mitochondrial energy regulation during oocyte activation, but mechanisms remain unclear.
Purpose of the Study:
- To investigate the roles of mitochondrial calcium channels in oocyte activation.
- To identify potential therapeutic targets for female infertility.
Main Methods:
- Inhibition of three mitochondrial calcium channels: Mitochondria Calcium Uniporter (MCU) using RU360, Sodium/Calcium Exchanger (NCLX) using CGP37157, and Voltage-dependent Calcium Channel (VDAC) using Erastin.
- Assessment of mitochondrial activity, intracellular calcium ([Ca2+]i), and intramitochondrial calcium ([Ca2+]m) oscillations.
- Monitoring of pronuclear formation and oocyte development.
Main Results:
- Inhibiting NCLX (CGP37157) and VDAC (Erastin) significantly reduced mitochondrial activity.
- Both NCLX and VDAC inhibition attenuated [Ca2+]i and [Ca2+]m oscillations.
- Disruption of these oscillations led to a developmental block in pronuclear formation.
Conclusions:
- NCLX and VDAC are key mitochondria-associated calcium transporters regulating oocyte activation.
- These channels are critical for maintaining calcium oscillations necessary for oocyte development.
- NCLX and VDAC represent potential therapeutic targets for treating female infertility.
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