LncRNA MALAT1 affects high glucose-induced endothelial cell proliferation, apoptosis, migration and angiogenesis by regulating the PI3K/Akt signaling pathway.

OBJECTIVE To investigate the effects of long non-coding ribonucleic acid (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the high glucose-induced proliferation, apoptosis, migration and angiogenesis of endothelial cells and its potential mechanism. MATERIALS AND METHODS Human umbilical vein endothelial cells (HUVECs) were divided into 3 groups, including control group (medium with 5.5 mmol/L glucose), high glucose group (HG group, medium with 33.5 mmol/L glucose) and lncRNA MALAT1 knockdown group [HG + MALAT1 small interfering RNA (siRNA) group, medium with 33.5 mmol/L glucose]. Cell Counting Kit-8 (CCK-8) assay was performed to observe the proliferation of HUVECs in each group at different time points. Meanwhile, the wound-healing assay was applied to detect the migratory ability of HUVECs in each group at 0 h and 24 h. The apoptosis rate of each group of cells was measured by means of flow cytometry, and the expression of Bcl-2-associated X protein (Bax) was detected via immunofluorescence at the same time. In addition, the amount of neovascularization in each group of cells was observed through the tube formation assay. Finally, Western blotting was utilized to determine the expression level of proteins in phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway in each group of cells. RESULTS Compared with that in the control group, the expression level of lncRNA MALAT1 in the HG group was elevated markedly (p<0.05). The proliferative capacity of HUVECs in the HG group was increased notably after knocking down lncRNA MALAT1 with siRNA (p<0.05). According to wound-healing assay, the knockdown of lncRNA MALAT1 could prominently reverse the declined HUVECs migratory ability induced by high glucose (p<0.05). Flow cytometry results manifested that the apoptosis level of HUVECs in the HG group was increased markedly, but inhibition on lncRNA MALAT1 could lower the apoptosis level evidently (p<0.05). The results of immunofluorescence showed that the expression of Bax in the HG + MALAT1 siRNA group was remarkably lower than that in the HG group (p<0.05). It was revealed in Western blotting that the knockdown of lncRNA MALAT1 could reverse the inhibition of high glucose on the PI3K/Akt signaling pathway in HUVECs (p<0.05). CONCLUSIONS Inhibiting lncRNA MALAT1 can promote endothelial cell proliferation, migration and angiogenesis and repress endothelial cell apoptosis simultaneously, whose mechanism may be related to the activation of the PI3K/Akt signaling pathway.