No abstract

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA (lncRNA), has been reported to potentially protect against cerebral ischemic injury. We investigated the role and underlying mechanism of MALAT1 in ischemic stroke. A mouse model of middle cerebral artery occlusion/reperfusion (MCAO/R) and a human brain microvascular endothelial cell (HBMEC) model of oxygen-glucose deprivation/reoxygenation (OGD/R) were established. The Zea Longa 5-point scale, VEGFR2/CD34 double immunofluorescence (IF), TUNEL staining, cell counting kit-8 (CCK-8) assay, tube formation assay, Transwell assay, and qRT–PCR were used to evaluate neurological deficits, endothelial cell (EC) proliferation, cell apoptosis, cell viability, in vitro angiogenesis, cell migration, and MALAT1 levels in mice, respectively. MALAT1 was found to promote cell migration and tube formation in vitro by affecting the caveolin-1/VEGF pathway. Downregulation of MALAT1 expression in vivo exacerbated cerebral ischemic injury as manifested by severe neurological deficits, elevation of apoptosis, and a decrease in the number of VEGFR2+/CD34+ endothelial progenitor cells (EPCs). These findings indicated that MALAT1 may promote angiogenesis after cerebral ischemic injury via the caveolin-1/VEGF pathway, thereby suggesting that MALAT1 is a therapeutic target for ischemic stroke.