ArticleMolecular neurobiology2024
GSK-126 Attenuates Cell Apoptosis in Ischemic Brain Injury by Modulating the EZH2-H3K27me3-Bcl2l1 Axis.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- JMJD3-driven epigenetic reprogramming of p16Bone research · 2026Article
- G9a Targeting by miR-122 Ameliorates Ischemic Brain Injury via Enhanced Microglial Autophagy and Suppressed Ferroptosis.Neurochemical research · 2026Article
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- LncRNA SNHG14 Regulates the Expression of BDNF by Recruiting Histone Methyltransferase EZH2 to Mediate H3K27me3, Thereby Affecting Angiogenesis and Functional Recovery After Cerebral Ischemia.Molecular neurobiology · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Whether epigenetic modifications participate in the cell apoptosis after ischemic stroke remains unclear. Histone 3 tri-methylation at lysine 27 (H3K27me3) is a histone modification that leads to gene silencing and is involved in the pathogenesis of ischemic stroke. Since the expression of many antiapoptotic genes is inhibited in the ischemic brains, here we aimed to offer an epigenetic solution to cell apoptosis after stroke by reversing H3K27me3 levels after ischemia. GSK-126, a specific inhibitor of enhancer of zeste homolog 2 (EZH2), significantly decreased H3K27me3 levels and inhibited middle cerebral artery occlusion (MCAO) induced and oxygen glucose deprivation (OGD) induced cell apoptosis. Moreover, GSK-126 attenuated the apoptosis caused by oxidative stress, excitotoxicity, and excessive inflammatory responses in vitro. The role of H3K27me3 in regulating of the expression of the antiapoptotic molecule B cell lymphoma-2 like 1 (Bcl2l1) explained the antiapoptotic effect of GSK-126. In conclusion, we found that GSK-126 could effectively protect brain cells from apoptosis after cerebral ischemia, and this role of GSK-126 is closely related to an axis that regulates Bcl2l1 expression, beginning with the regulation of EZH2-dependent H3K27me3 modification.
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