ArticleJournal of molecular neuroscience : MN2020
Alpha B-Crystallin Overexpression Protects Oligodendrocyte Precursor Cells Against Oxidative Stress-Induced Apoptosis Through the Akt Pathway.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanism analysis and intervention strategies of the inflammatory microenvironment in traumatic spinal cord injury.Frontiers in immunology · 2025Review
- The pathogenesis of multiple sclerosis: a series of unfortunate events.Clinical and experimental immunology · 2023Article
- Interplay between Nrf2 and αB-crystallin in the lens and heart of zebrafish under proteostatic stress.Frontiers in molecular biosciences · 2023Article
- Ultrafine Diesel Exhaust Particles Induce Apoptosis of Oligodendrocytes by Increasing Intracellular Reactive Oxygen Species through NADPH Oxidase Activation.Antioxidants (Basel, Switzerland) · 2022Article
- Calpain-mediated protein targets in cardiac mitochondria following ischemia-reperfusion.Scientific reports · 2022Article
- Study on the Anti-demyelination Mechanism of Bu-Shen-Yi-Sui Capsule in the Central Nervous System Based on Network Pharmacology and Experimental Verification.Mediators of inflammation · 2022Article
- High Vulnerability of Oligodendrocytes to Oxidative Stress Induced by Ultrafine Urban Particles.Antioxidants (Basel, Switzerland) · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alpha B-crystallin (aBC), a member of the small heat shock protein family, is expressed in mature oligodendrocytes (mOLs), but not in oligodendrocyte precursor cells (OPCs). Our previous study found that the survival rate of OPCs was lower than that of mOLs under oxidative stress, suggesting that aBC may play a protective role in mOLs. In the present study, we investigated the effects of aBC overexpression on oxidative stress-induced cell injury in OPCs and examined the underlying mechanisms. We observed that the survival rates of aBC-overexpressed OPCs were significantly higher than those of control cells under oxidative stress induced by hydrogen peroxide. Akt activities were significantly suppressed by oxidative stress in control OPCs, but not in aBC-overexpressed OPCs. The expressions of Bax and cleaved caspase-3 were decreased, whereas Bcl-2 expression was increased in aBC-overexpressed OPCs under oxidative stress. These findings suggest that low Akt activity in OPCs due to aBC deficiency may cause high susceptibility of OPCs to oxidative stress. The findings may provide new insights into the implication of OPCs in demyelinating diseases.
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Registered trials
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