4.6 Article

2-Mercaptoethanol promotes porcine oocyte maturation in vitro by maintaining autophagy homeostasis

Journal

THERIOGENOLOGY
Volume 186, Issue -, Pages 155-167

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.theriogenology.2022.04.009

Keywords

Porcine; Oocyte; 2-Mercaptoethanol; Autophagy disorders; In vitro maturation; Protective effects

Funding

  1. Guangxi Science Foundation Program, China [2018GXNSFDA050013]
  2. National Nat-ural Science Foundation of China [31872350]

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This study found that 2-Mercaptoethanol (2-ME) can promote in vitro maturation of porcine oocytes by maintaining autophagy homeostasis, leading to improved embryo development.
2-Mercaptoethanol (2-ME) is often used as an antioxidant to optimize culture systems for in vitro oocyte maturation in livestock. However, the relationship between 2-ME and autophagy has not yet been elucidated. In this study, we hypothesized that 2-ME can promote porcine oocyte maturation in vitro by maintaining autophagy homeostasis. To test this hypothesis, we explored the effects of 2-ME on the maturation of porcine oocytes exposed to an autophagy activator (rapamycin) or an autophagy inhibitor (3-methyladenine, i.e., 3-MA) in vitro. Rapamycin-induced autophagy over-activation significantly increased autophagy- and apoptosis-related gene expression, oxidative stress, apoptosis rates, abnormal mitochondrial redistribution, and significantly decreased oocyte first polar body extrusion (PBE) rates, spindle/chromosome integrity and developmental competence. 3-MA-mediated autophagy inhibition exerted similar effects on all these parameters except the expression of genes that promote autophagy and inhibit apoptosis. Importantly, 2-ME supplementation significantly attenuated the detrimental effects of rapamycin and 3-MA. Interestingly, we observed that 44 h of coincubation with rapamycin/3-MA and 2-ME restored autophagy homeostasis in vitro. In conclusion, our study confirmed that 2-ME promotes porcine oocyte maturation and embryo development in vitro by maintaining autophagy homeostasis and lays a foundation for further research on the underlying mechanism. (c) 2022 Elsevier Inc. All rights reserved.

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