MiR-122-5p Attenuates Endothelial-to-Mesenchymal Transition Induced by Oxygen and Glucose Deprivation/Reperfusion

Endothelial-to-mesenchymal transition (EndoMT) is a common phenomenon in vascular diseases, while the role of endothelial dysfunction central disease remains to be further investigated. MiR-122 an inflammation-associated non-coding RNA that participates multiple human disease, but whether miR-122 plays as critical EndoMT induced by ischaemic stroke unknown. Although BAI2 known brain-specific inhibitor protein angiogenesis, few studies examined EndoMT. This study investigated mechanism and miR-122/BAI2 axis oxygen-glucose deprivation/reperfusion (OGD/R)-mediated A transient middle cerebral artery occlusion (tMCAO) model OGD/R treatment were used mimic ischaemia-reperfusion injury. The colocalization CD31 α-SMA was elevated peri-infarct area tMCAO mice. expression decreased Downregulation miR-122, Occludin, ZO-1 observed brain microvascular cells (HBMECs) after treatment, increased HBMECs treatment. overexpression reduced decrease Occludin increase OGD/R. negatively regulated expression, enhanced expression. Knockdown suppressed In conclusion, attenuates OGD/R-mediated targeting BAI2.