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Nampt affects mitochondrial function in aged oocytes by mediating the downstream effector FoxO3a.
Qingrui Zhuan1, Jun Li2, Xingzhu Du1
1National Engineering Laboratory for Animal Breeding, Beijing Key Laboratory for Animal Genetic Improvement, College of Animal Science and Technology, China Agricultural University, Beijing, China.
Journal of Cellular Physiology
|July 28, 2021
Summary
Maternal aging impairs oocyte quality, increasing reactive oxygen species and altering protein levels like FoxO3a. Suppressing Nampt further damages mitochondrial function in aged oocytes.
Area of Science:
- Reproductive Biology
- Cellular Aging
- Mitochondrial Biology
Background:
- Maternal aging negatively impacts oocyte quality and developmental potential.
- Oocyte aging is associated with cellular stress, including increased reactive oxygen species (ROS).
Purpose of the Study:
- To investigate the effects of maternal aging on oocyte quality and mitochondrial function in mice.
- To explore the roles of Forkhead box O3a (FoxO3a) and nicotinamide-phosphoribosyltransferase (Nampt) in aged oocytes.
Main Methods:
- Comparative analysis of oocytes from young and aged mice.
- Measurement of reactive oxygen species (ROS), mitochondrial calcium (Ca2+), and temperature.
- Assessment of FoxO3a and Nampt expression and localization.
- Pharmacological manipulation of Nampt activity using P7C3 and FK866.
Main Results:
- Aged oocytes exhibited compromised germinal vesicle breakdown (GVBD), elevated ROS, and altered mitochondrial Ca2+ and temperature.
- FoxO3a expression and nuclear localization increased in aged oocytes.
- Nampt expression was upregulated in aged oocytes and ovaries, peaking during GVBD.
- FK866 treatment significantly reduced ATP levels and mitochondrial membrane potential in aged oocytes.
Conclusions:
- Mitochondrial dysfunction in aged oocytes is linked to elevated FoxO3a levels.
- Suppression of Nampt exacerbates mitochondrial dysfunction in aged oocytes, highlighting its critical role.
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