DOI: 10.1097/wnr.0000000000002274 ISSN: 0959-4965
LINC01128 alleviates neuronal injury and neurological deficits after ischemic stroke via targeting miR-92a-3p
Jing Xiao, Jianjian Zhu
Background
Ischemic stroke is a severe cerebrovascular disease. Focusing on ischemic stroke, this study aims to determine
LINC01128
expression changes and its mechanism involving miR-92a-3p regulation.
Methods
A rat model of middle cerebral artery occlusion and an oxygen–glucose deprivation/reoxygenation model of SH-SY5Y cells were established to simulate ischemic stroke. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of
LINC01128
and miR-92a-3p. Dual luciferase reporter gene, RNA immunoprecipitation, and RNA pull-down experiments were used to verify the molecular interactions. ELISA and reactive oxygen species (ROS) assays were used to evaluate the levels of inflammation and oxidative stress. The neurological function was evaluated by foot fault test, corner test, and modified neurological severity score.
Results
LINC01128
expression was markedly decreased, whereas miR-92a-3p expression was increased in ischemic stroke models. Experiments confirmed that
LINC01128
directly binds to miR-92a-3p. In-vivo models demonstrated that
LINC01128
overexpression effectively reduced proinflammatory factor levels and ROS production, increased the anti-inflammatory factor, and improved neurological dysfunction. Overexpression of
LINC01128
also mitigated oxygen–glucose deprivation/reoxygenation-induced apoptosis, inflammation, and intracellular ROS accumulation while enhancing cell viability. However, all these protective effects were reversed by co-overexpression of miR-92a-3p.
Conclusion
LINC01128
exerts a crucial neuroprotective effect in ischemic stroke models by targeting miR-92a-3p, effectively alleviating neuroinflammation and oxidative stress damage while improving neurological deficits. The discovery of the
LINC01128
/miR-92a-3p regulatory axis provides new insights into the molecular mechanisms underlying poststroke neural injury.