Research Paper Volume 8, Issue 4 pp 685—694
SIRT1, 2, 3 protect mouse oocytes from postovulatory aging
- 1 Institute of Reproductive Sciences, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, China
- 2 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
- 3 Department of Reproductive Medicine, Guangdong Women and Children Hospital, Guangzhou, China
- 4 Department of Reproductive Medicine, Peking University Shenzhen Hospital, Medical Center of Peking University, Shenzhen, Guangdong, China
- 5 Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211, USA
Received: October 6, 2015 Accepted: January 30, 2016 Published: March 10, 2016
https://doi.org/10.18632/aging.100911How to Cite
Abstract
The quality of metaphase II oocytes will undergo a time-dependent deterioration following ovulation as the result of the oocyte aging process. In this study, we determined that the expression of sirtuin family members (SIRT1, 2, 3) was dramatically reduced in mouse oocytes aged in vivo or in vitro. Increased intracellular ROS was observed when SIRT1, 2, 3 activity was inhibited. Increased frequency of spindle defects and disturbed distribution of mitochondria were also observed in MII oocytes aged in vitro after treatment with Nicotinamide (NAM), indicating that inhibition of SIRT1, 2, 3 may accelerate postovulatory oocyte aging. Interestingly, when MII oocytes were exposed to caffeine, the decline of SIRT1, 2, 3 mRNA levels was delayed and the aging-associated defective phenotypes could be improved. The results suggest that the SIRT1, 2, 3 pathway may play a potential protective role against postovulatory oocyte aging by controlling ROS generation.