ArticleBioscience reports2020
UCH-L1 inhibitor LDN-57444 hampers mouse oocyte maturation by regulating oxidative stress and mitochondrial function and reducing ERK1/2 expression.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Curcumin-Loaded Milk-Derived Exosomes Improve the Developmental Competence of Yak Oocytes by Regulating Mitophagy.Antioxidants (Basel, Switzerland) · 2026Article
- Effect of Melatonin and Epigallocatechin-3-Gallate Combination on In Vitro Maturation of Mouse Oocytes.International journal of molecular sciences · 2026Article
- Ubiquitin C-terminal hydrolase L1 (UCHL1), a double-edged sword in mammalian oocyte maturation and spermatogenesis.Cell proliferation · 2023Review
- Role of the deubiquitinating enzyme UCH-L1 in mitochondrial function.Frontiers in cellular neuroscience · 2023Article
- The requirement of ubiquitin C-terminal hydrolase L1 in mouse ovarian development and fertility†.Biology of reproduction · 2022Article
- Quantitative proteomic analysis after neuroprotective MyD88 inhibition in the retinal degeneration 10 mouse.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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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.
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