UCH-L1 inhibitor LDN-57444 hampers mouse oocyte maturation by regulating oxidative stress and mitochondrial function and reducing ERK1/2 expression. Issue 10 (30th October 2020)

• Record Type: Journal Article
• Authors: Yuan, Pan; Zhou, Li; Zhang, Xiaona; Yao, Lan; Ning, Jun; Han, Xiao; Ming, Caifeng; Zhao, Yunhe; Zhang, Liqun
• Is Part Of: Bioscience reports. Volume 40:Issue 10(2020)
• Publication Date: 2020-10-30
• Subjects: maturation -- mouse -- oocytes -- oxidative stress -- spindle body -- UCH-L1; Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1042/BSR20201308
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract: Oocyte maturation is a prerequisite for successful fertilization and embryo development. Incomplete oocyte maturation can result in infertility. Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) has been found to be implicated in oocyte maturation and embryo development. However, the cellular and molecular mechanisms of UCH-L1 underlying oocyte maturation have not been fully elucidated. In the present study, we observed that the introduction of UCH-L1 inhibitor LDN-57444 suppressed first polar body extrusion during mouse oocyte maturation. The inhibition of UCH-L1 by LDN-57444 led to the notable increase in reactive oxygen species (ROS) level, conspicuous reduction in glutathione (GSH) content and mitochondrial membrane potential (MMP), and blockade of spindle body formation. As a conclusion, UCH-L1 inhibitor LDN-57444 suppressed mouse oocyte maturation by improving oxidative stress, attenuating mitochondrial function, curbing spindle body formation and down-regulating extracellular signal-related kinases (ERK1/2) expression, providing a deep insight into the cellular and molecular basis of UCH-L1 during mouse oocyte maturation.