Endoplasmic reticulum stress inhibition is a valid therapeutic strategy in vitrifying oocytes

• Published in: Cryobiology 2015-02, Vol.70 (1), p.48-52
• Main Authors: Zhao, Nan, Liu, Xue-Jun, Li, Jun-Tao, Zhang, Ling, Fu, Yang, Zhang, Ya-Jie, Chen, Ru-Xin, Wei, Xiao-Qing, Wang, Rui, Wang, Yu, Zhang, Jian-Min
• Format: Article
• Language: English
• Subjects: Animals; Caspase 12 - biosynthesis; Caspase-12; Cell Survival; Cryopreservation - methods; DNA-Binding Proteins - biosynthesis; Endoplasmic reticulum stress; Endoplasmic Reticulum Stress - drug effects; Female; Mice; Mice, Inbred ICR; Oocytes; Oocytes - physiology; Regulatory Factor X Transcription Factors; Taurochenodeoxycholic Acid - pharmacology; Transcription Factors - biosynthesis; Tunicamycin - pharmacology; Vitrification; X-Box Binding Protein 1
• ISSN: 0011-2240; 1090-2392
• DOI: 10.1016/j.cryobiol.2014.12.001

The aim of this study is to determine the link between oocyte cryopreservation and endoplasmic reticulum (ER) stress; whether ER stress inhibition improves the efficiency of oocyte vitrification is also explored. Oocytes from mice were exposure to tauroursodeoxycholic acid (TUDCA, an ER stress inhibitor) or TM (tunicamycin, an ER stress inducer) with or without vitrification. The expressions of X-box binding protein-1 (XBP-1) protein and caspase-12 protein, viability of vitrified-warmed oocytes, and their subsequent embryo competence were measured. The levels of XBP-1 protein and caspase-12 protein expression in vitrified-warmed oocytes were significantly higher than those of fresh control oocytes. TUDCA improved the viability of vitrified-warmed oocytes and their subsequent embryo competence. Mouse oocyte cryopreservation is associated with ER stress, and ER stress inhibition improves the efficiency of oocyte vitrification.