MALAT1 Protected the Angiogenesis Function of Human Brain Microvascular Endothelial Cells (HBMECs) Under Oxygen Glucose Deprivation/re-oxygenation (OGD/R) Challenge by Interacting with miR-205-5p/VEGFA Pathway.

Long non-coding RNA MALAT1 was previously revealed to express abnormally in animal and cellular models of stroke, suggesting its indispensable role in stroke. The aims of the present study were to further investigate the functions of MALAT1 and to elucidate the underlying molecular mechanisms. Oxygen glucose deprivation/re-oxygenation (OGD/R) challenge was used in human brain microvascular endothelial cells (HBMECs) to mimic stroke injury in vitro. MALAT1 and miR-205-5p expression levels were evaluated by qRT-PCR. A tube formation assay was employed to verify the angiogenesis of HBMECs. Cell proliferation and apoptosis were evaluated using the ErdU assay and flow cytometry analysis, respectively. The interaction between miR-205-5p and MALAT1 was verified by dual-luciferase reporter assay. MALAT1 and miR-205-5p were both significantly upregulated in the serum of CIS patients and HBMECs under OGD/R, and the tube formation of HBMECs was damaged after OGD/R treatment. Silencing miR-205-5p remarkably promoted HBMEC proliferation and angiogenesis to resist OGD/R injury. Knockdown of MALAT1 markedly inhibited HBMEC proliferation and angiogenesis, and meanwhile promoted apoptosis induced by OGD/R treatment. Most importantly, MALAT1 acted as a competing endogenous RNA (ceRNA) of miR-205-5p via direct bonding with each other in HBMECs under OGD/R damage, indirectly upregulating the downstream targeted gene VEGFA. MALAT1 protected the angiogenesis function of HBMECs under OGD/R conditions by interacting with miR-205-5p/VEGFA pathway.