TGF-β1 upregulates the expression of lncRNA-ATB to promote atherosclerosis

Transforming growth factor (TGF)-β1 is reported to be associated with the occurrence of atherosclerosis, although the mechanism remains unclear. Therefore, the present study aimed to investigate the involvement of TGF-β1 signaling in atherosclerosis. A total of 56 patients with atherosclerosis and 44 healthy volunteers were involved in this study. Serum expression of TGF-β1 and long non-coding RNA-ATB was detected by ELISA and quantitative polymerase chain reaction (qPCR). Receiver operating characteristic curve analysis was performed to analyze the diagnostic value of serum TGF-β1 and lncRNA-ATB for atherosclerosis. A human umbilical vein endothelial cell (HUVEC) line overexpressing lncRNA-ATB was constructed. The effects of TGF-β1 treatment and lncRNA-ATB overexpression on HUVEC cell proliferation and viability was detected with Cell Counting Kit-8 and MTT assays, respectively. Expression of TGF-β1 and pro-apoptotic Caspase-3 in lncRNA-ATB-overexpressing HUVECs was detected by western blotting. In addition, the expression of lncRNA-ATB in TGF-β1-treated HUVECs was detected by qPCR. It was demonstrated that serum TGF-β1 and lncRNA-ATB expression was significantly higher in atherosclerosis patients, compared with controls, and could be used to effectively distinguish patients from healthy individuals. TGF-β1 treatment and lncRNA-ATB overexpression reduced HUVEC viability and proliferation. TGF-β1 treatment increased the expression of lncRNA-ATB in HUVECs, while lncRNA-ATB overexpression had no significant effect on TGF-β1 expression. LncRNA-ATB silencing with small interfering RNA significantly reduced the effects of TGF-β1 treatment on the proliferation and viability of HUVECs. Furthermore, LncRNA-ATB overexpression upregulated the expression of caspase-3 in HUVECs. Therefore, it was concluded that TGF-β1 may have upregulated the expression of lncRNA-ATB to promote atherosclerosis, and lncRNA-ATB may serve as a potential therapeutic target for atherosclerosis. However, the mechanism remains to be further investigated.