Open AccessSilencing miRNA-324-3p protects against cerebral ischemic injury via regulation of the GATA2/A1R axis
Author(s) -
Yunchang Mo,
Qinxue Dai,
Junlu Wang,
Anqi Zhang,
Lu Wang,
Yixiu Wang,
Shanshan Hong,
Yu-Shan Zhong,
Ru-Yi Yu,
Xinlu Wu,
Bingbing Zhou,
Qian Yu,
Haifeng Fu,
Shuangdong Chen
Publication year - 2022
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.339009
Subject(s) - gene silencing , ischemia , apoptosis , microrna , medicine , pharmacology , brain damage , in vivo , stroke (engine) , viability assay , cancer research , anesthesia , biology , biochemistry , gene , genetics , mechanical engineering , engineering
Previous studies have suggested that miR-324-3p is related to the pathophysiology of cerebral ischemia, but the mechanism underlying this relationship is unclear. In this study, we found that miR-324-3p expression was decreased in patients with acute ischemic stroke and in in vitro and in vivo models of ischemic stroke. miR-324-3p agomir potentiated ischemic brain damage in rats subjected to middle cerebral artery occlusion, as indicated by increased infarct volumes and cell apoptosis rates and greater neurological deficits. In a PC12 cell oxygen-glucose deprivation/reoxygenation model, a miR-324-3p mimic decreased cell viability and expression of the anti-apoptotic protein BCL2 and increased expression of the pro-apoptotic protein BAX and rates of cell apoptosis, whereas treatment with a miR-324-3p inhibitor had the opposite effects. Silencing miR-324-3p increased adenosine A1 receptor (A1R) expression through regulation of GATA binding protein 2 (GATA2). These findings suggest that silencing miR-324-3p reduces ischemic brain damage via the GATA2/A1R axis.