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.