Research Paper|Volume 8, Issue 4|pp 685—694

SIRT1, 2, 3 protect mouse oocytes from postovulatory aging

Teng Zhang^1,², Yang Zhou², Li Li^2,³, Hong-Hui Wang^1,², Xue-Shan Ma², Wei-Ping Qian⁴, Wei Shen¹, Heide Schatten⁵, Qing-Yuan Sun^1,²

¹Institute of Reproductive Sciences, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, China
²State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
³Department of Reproductive Medicine, Guangdong Women and Children Hospital, Guangzhou, China
⁴Department of Reproductive Medicine, Peking University Shenzhen Hospital, Medical Center of Peking University, Shenzhen, Guangdong, China
⁵Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211, USA

Received: October 6, 2015Accepted: January 30, 2016Published: March 10, 2016

https://doi.org/10.18632/aging.100911

Copyright: © 2016 Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.