LncRNA FGD5-AS1 reduces ox-LDL-induced damage of HUVECs by targeting miR-106a-5p

Objective To explore the effect of lncRNA FGD5-AS1 on oxidized low-density lipoprotein (ox-LDL)-induced vascular endothelial cell damage and its regulatory effect on miR-106a-5p. Methods Ox-LDL was used to induce human umbilical vein endothelial cells(HUVECs) to establish a cellular injury model. pcDNA-FGD5-AS1, anti-miR-106a-5p and its negative control were transfected into HUVECs and then added to ox-LDL-treated cells. pcDNA-FGD5-AS1 was co-transfected with miR-NC and miR-106a-5p mimics to HUVECs, then added ox-LDL to treat cells. RT-qPCR was used to detect the expression of FGD5-AS1 and miR-106a-5p. The level of MDA, SOD, and CAT was tested with commercially available kit. Flow cytometry was used to detect the apoptosis rate. The dual luciferase reporter gene experiment was used to detect the targeting relationship between FGD5-AS1 and miR-106a-5p. Western blot was used to detect the protein expression of cleaved caspase-3 and cleaved caspase-9. Results The expression of FGD5-AS1 mRNA in HUVECs induced by ox-LDL decreased (P＜0.05) while the expression of miR-106a-5p mRNA increased (P＜0.05). Both transfection of pcDNA-FGD5-AS1 and transfection of anti-miR-106a-5p reduced the level of MDA, apoptosis rate and protein level of cleaved caspase-3, cleaved caspase-9 in HUVECs induced by ox-LDL(P＜0.05),enhanced the activity of SOD and CAT (P＜0.05). FGD5-AS1 could target at miR-106a-5p. Co-transfection of pcDNA-FGD5-AS1 and miR-106a-5p mimics could reverse the effect of pcDNA-FGD5-AS1 on ox-LDL-induced HUVECs apoptosis and oxidative stress. Conclusions Over-expression of FGD5-AS1 may inhibit oxidative stress and apoptosis through targeted regulation of miR-106a-5p, thereby reducing ox-LDL-induced vascular endothelial cell damage.