ArticleMolecular neurobiology2026
H3K27ac-Activated lncRNA-DAPK1-IT1 Aggravated Oxidative Stress Damage Induced by Focal Cerebral Ischemia/Reperfusion via the miR-25-3p/HMGB1 Molecular Axis.
Article in Molecular neurobiology, 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
Ischemic stroke is a prevalent neurological disorder, characterized by elevated mortality and significant long-term disability. Oxidative stress damage is an important pathological process that occurs after brain ischemia/reperfusion (I/R), in which the long non-coding RNA death-associated protein kinase 1 intronic transcript 1 (DAPK1-IT1) is aberrantly expressed and participates in oxidative stress damage; however, its specific mechanisms of action remain unclear. DAPK1-IT1 and miR-25-3p expression was detected using qRT-PCR in the mouse neuroblastoma N2a cells that received middle cerebral artery occlusion/reperfusion and oxygen-glucose deprivation/reperfusion. Functional gain and loss experiments were performed to manipulate DAPK1-IT1, miR-25-3p, and HMGB1 expression. The role of DAPK1-IT1 was assessed both in vivo and in vitro using CCK-8, flow cytometry, and western blotting. The results showed that the levels of DAPK1-IT1, HMGB1, and oxidative stress damage markers were significantly increased, whereas miR-25-3p expression was significantly downregulated. The expression levels of DAPK1-IT1 were positively correlated with ROS production. DAPK1-IT1 and HMGB1 were identified as potential targets of miR-25-3p. Knockdown of DAPK1-IT1 and HMGB1, as well as overexpression of miR-25-3p, is indeed protective and contribute to reducing oxidative stress damage by activating the Nrf2/HO-1 signaling pathway. DAPK1-IT1 overexpression caused oxidative stress damage in N2a cells by downregulating miR-25-3p expression and upregulating HMGB1 expression. Mechanistically, DAPK1-IT1 upregulated HMGB1 expression by sponging miR-25-3p and mediating histone H3 lysine 27 acetylation in the promoter region through the cAMP response element-binding protein-binding protein (CBP). In summary, we found that H3K27 acetylation-induced lncRNA-DAPK1-IT1 promotes oxidative stress damage caused by I/R through the miR-25-3p/HMGB1 axis. These findings help to improve our understanding of ischemic stroke and provide new therapeutic avenues.
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