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.
Highlights
Oocytes, female gametocytes or germ cells involved in reproduction, can transmit maternal nuclear and mitochondrial genome information to the embryo and determine embryo developmental potential in women [1]
Since Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) is a component of ubiquitin proteasome system, the effect of LDN-57444 on proteasome activity was further measured in mouse oocytes
We demonstrated that the introduction of UCH-L1 inhibitor LDN-57444 suppressed mouse oocyte maturation by improving oxidative stress, inducing mitochondrial dysfunction, curbing spindle body formation, and reducing extracellular signal-related kinase (ERK1/2) protein expression
Summary
Female gametocytes or germ cells involved in reproduction, can transmit maternal nuclear and mitochondrial genome information to the embryo and determine embryo developmental potential in women [1]. Preovulatory luteinizing hormone outpouring induces meiosis resumption and progression till oocyte maturation (metaphase II (MII) stage). In vitro maturation (IVM) of immature oocytes, a vital technique in fertility preservation, has attracted much attention from researchers in recent years due to its specific advantages [4,5]. This technique requires no or little gonadotropin supplementation in vivo, which can significantly reduce ovarian hyperstimulation syndrome risk, medical expenses and drug-related side effects [5,6]. An in-depth understanding on cellular and molecular basis of oocyte IVM contributes to fertility protection, pregnancy rate improvement and the better management of ovarian hyperstimulation syndrome and infertility
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