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Loss of TIGAR Induces Oxidative Stress and Meiotic Defects in Oocytes from Obese Mice
Haichao Wang1, Qing Cheng2, Xiaoyan Li1,3
1From the ‡State Key Laboratory of Reproductive Medicine, Nanjing Medical University.
Abstract:
Maternal obesity has been reported to impair oocyte quality in mice, however, the underlying mechanisms remain unclear. In the present study, by conducting a comparative proteomic analysis, we identified a reduced expression of TIGAR (TP53-induced glycolysis and apoptosis regulator) protein in ovulated oocytes from high-fat diet (HFD)-fed mice. Specific depletion of TIGAR in mouse oocytes results in the marked elevation of reactive oxygen species (ROS) levels and the failure of meiotic apparatus assembly. Importantly, forced expression of TIGAR in HFD oocytes not only attenuates ROS production, but also partly prevents spindle disorganization and chromosome misalignment during meiosis. Meantime, we noted that TIGAR knockdown in oocytes induces a strong activation of autophagy, whereas overexpression of TIGAR significantly reduces the LC3 accumulation in HFD oocytes. By anti-oxidant treatment, we further demonstrated that such an autophagic response is dependent on the TIGAR-controlled ROS production. In summary, our data indicate a role for TIGAR in modulating redox homeostasis during oocyte maturation, and uncover that loss of TIGAR is a critical pathway mediating the effects of maternal obesity on oocyte quality.
Insights
Maternal obesity impairs egg quality by reducing TIGAR (TP53-induced glycolysis and apoptosis regulator) protein. Loss of TIGAR increases oxidative stress and disrupts egg maturation, highlighting its role in fertility.
Area of Science:
- Reproductive Biology
- Molecular Endocrinology
- Cellular Metabolism
Background:
- Maternal obesity is linked to reduced oocyte quality, but mechanisms are poorly understood.
- TP53-induced glycolysis and apoptosis regulator (TIGAR) protein's role in oocyte health is unexplored.
Purpose of the Study:
- Investigate the role of TIGAR in maternal obesity-induced oocyte quality decline.
- Elucidate the mechanisms by which TIGAR affects oocyte maturation and redox homeostasis.
Main Methods:
- Comparative proteomic analysis of oocytes from high-fat diet (HFD) fed mice.
- TIGAR depletion and overexpression in mouse oocytes.
- Assessment of reactive oxygen species (ROS) levels, meiotic apparatus assembly, and autophagy markers (LC3).
Main Results:
- Reduced TIGAR expression observed in oocytes from HFD-fed mice.
- TIGAR depletion elevated ROS and impaired meiotic spindle assembly.
- TIGAR overexpression attenuated ROS and improved meiotic progression in HFD oocytes.
- TIGAR levels inversely correlated with autophagy activation (LC3 accumulation).
Conclusions:
- TIGAR plays a crucial role in maintaining redox homeostasis during oocyte maturation.
- Loss of TIGAR is a key mediator of adverse effects of maternal obesity on oocyte quality.
- TIGAR-controlled ROS production influences the autophagic response in oocytes.
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