ArticleMolecular biology reports2026
BTG2 knockdown attenuates oxygen-glucose deprivation/reoxygenation-induced injury and apoptosis in PC12 cells: an effect associated with MAPK pathway inhibition.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundApoptosis, oxidative stress, and inflammatory responses are involved in ischemia-reperfusion injury (IRI), a pathological process leading to neuronal damage. B-cell translocation gene 2 (BTG2) regulates cellular injury and apoptosis. However, its role and molecular mechanisms in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury remain unclear.
objectiveTo explore BTG2's role in OGD/R-induced injury in PC12 cells and its underlying mechanism.
methodsDifferentially expressed genes (DEGs) in OGD/R-treated PC12 cells were identified. Key pathways were screened out using GO and KEGG. BTG2 expression was silenced using RNA interference. The phosphorylation levels of proteins associated with the mitogen-activated protein kinase (MAPK) pathway were further examined. Rescue experiments were performed using anisomycin, a MAPK pathway activator, to verify the functional involvement of MAPK pathway in BTG2-mediated effects.
resultsDEGs (n = 115) were identified through bioinformatics analysis, which were mainly enriched in cellular stress responses, cell cycle regulation, and apoptosis-related processes. OGD/R treatment significantly upregulated BTG2 expression in PC12 cells. BTG2 knockdown markedly alleviated OGD/R-induced PC12 cell injury. Mechanistically, BTG2 knockdown significantly suppressed MAPK pathway activation induced by OGD/R. Reactivation of the MAPK pathway by anisomycin partially reversed the protective effects conferred by BTG2 knockdown.
conclusionBTG2 promotes apoptosis, oxidative stress, and inflammatory responses in OGD/R-induced PC12 cell injury, at least partly associated with the activation of the MAPK pathway.
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