Downregulation of lncRNA H19 alleviates atherosclerosis through inducing the apoptosis of vascular smooth muscle cells
- Hui Sun
- Qianqian Jiang
- Li Sheng
- Kai Cui
Affiliations: Department of Cardiology, Jining First People's Hospital, Jining, Shandong 272100, P.R. China, Department of Cardiology, The Second People's Hospital of Liaocheng, Linqing, Liaocheng, Shandong 252601, P.R. China, Geriatrics Department, The Central Hospital of Shengli Oilfield, Dongying, Shandong 257034, P.R. China
- Published online on: July 31, 2020 https://doi.org/10.3892/mmr.2020.11394
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Aberrant proliferation and apoptosis of vascular smooth muscle cells (VSMCs) serve a dominant role in the pathogenesis of atherosclerosis (AS). Long non‑coding (lnc)RNA H19 is reported to accelerate the progression of AS by inhibiting the apoptosis of VSMCs, whereas p53 is identified as promoting VSMC apoptosis. The present study aimed to explore the effects of H19/p53 on the pathogenesis of AS. Apolipoprotein E knockout (ApoE‑/‑) mice fed a high‑fat diet were used as in vivo AS models. Reverse transcription‑quantitative PCR and western blot were used to detect mRNA and protein expression levels, respectively. VSMC proliferation and apoptosis were respectively assessed by CCK‑8 and flow cytometry. Compared with the control group, mouse weight and plaque area were all increased in the AS model group, as was the expression of H19. Knockdown of H19 reduced the proliferation and induced apoptosis of VSMCs, and increased the expression of p53, cleaved caspase3 (c‑caspase3) and p53 upregulated modulator of apoptosis, as well as enhancing the interaction between Bax and p53 proteins. Downregulation of H19 reduced the plaque area and promoted the expression of c‑caspase3 in mouse aortic tissues in vivo, as well as enhancing the effects of simvastatin, a drug used for AS treatment. Results from the present study indicated that knockdown of H19 may prevent AS deterioration through increased p53‑mediated VSMC apoptosis.