Journal
MOLECULAR NEUROBIOLOGY
Volume 60, Issue 10, Pages 6109-6120Publisher
SPRINGER
DOI: 10.1007/s12035-023-03450-4
Keywords
Ischemic stroke; OGD; R; Cerebral injury; LncRNA XIST; MiR-25-3p; TRAF3
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Ischemic stroke causes lethal damage to the brain, and identifying key regulators of OGD/R-induced cerebral injury is crucial for developing novel therapies. This study found that LncRNA XIST exacerbates OGD/R-induced cerebral damage by acting as a sponge for miR-25-3p and enhancing TRAF3 expression.
Ischemic stroke causes lethal damage to the brain. Identifying key regulators of OGD/R-induced cerebral injury is important for developing novel therapies for ischemic stroke. HMC3 and SH-SY5Y cells were treated with OGD/R as an in vitro ischemic stroke model. Cell viability and apoptosis were determined via CCK-8 assay and flow cytometry. Inflammatory cytokines were examined by ELISA. Luciferase activity was measured for evaluating the interaction of XIST, miR-25-3p, and TRAF3. Bcl-2, Bax, Bad, cleaved-caspase 3, total caspase 3, and TRAF3 were detected via western blotting. HMC3 and SH-SY5Y cells showed increased XIST expression and decreased miR-25-3p expression following OGD/R. Importantly, silencing of XIST and overexpression of miR-25-3p reduced apoptosis and inflammatory response following OGD/R. Furthermore, XIST worked as a miR-25-3p sponge, and miR-25-3p targeted TRAF3 to suppress its expression. Moreover, the knockdown of TRAF3 ameliorated OGD/R-induced injury. Loss of XIST-mediated protective effects was reversed by overexpression of TRAF3. LncRNA XIST exacerbates OGD/R-induced cerebral damage via sponging miR-25-3p and enhancing TRAF3 expression.
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