miR‑129‑5p inhibits oxidized low‑density lipoprotein‑induced A7r5 cell viability and migration by targeting HMGB1 and the PI3k/Akt signaling pathway
- Hongfei Jiang
- Ren Gong
- Yanqing Wu
Affiliations: Department of Cardiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
- Published online on: January 27, 2022 https://doi.org/10.3892/etm.2022.11168
Copyright: © Jiang
et al. This is an open access article distributed under the
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The mechanisms underlying gene therapy for the treatment of cardiovascular diseases remain to be elucidated. microRNAs (miRs) have been recognized as key regulators in vascular smooth muscle cells, which are involved in the formation of atherosclerosis. The present study aimed to explore the role of miR‑129‑5p in the regulation of high‑mobility group box 1 protein (HMGB1) and the PI3k/Akt signaling pathway, and further explore the role of miR‑129‑5p in the viability and migration of A7r5 cells induced by oxidized low‑density lipoprotein (ox‑LDL). Cell viability, viability and migration were determined using Cell Counting Kit‑8, colony formation, wound healing and Transwell assays. The expression levels of miR‑129‑5p and HMGB1 were detected using reverse transcription‑quantitative PCR and western blotting. A dual‑luciferase assay was used to confirm the association between miR‑129‑5p and HMGB1. RT‑qPCR results in the present study demonstrated that the expression levels of miR‑129‑5p in A7r5 cells induced by ox‑LDL were significantly decreased, compared with the control cells. Moreover, the viability and migration of A7r5 cells induced by ox‑LDL were increased compared with control group. Western blot and RT‑qPCR results showed that miR‑129‑5p decreased the expression of HMGB1 in A7r5 cells compared with control group. The present results demonstrated that miR‑129‑5p inhibited the viability, viability and migration of A7r5 cells induced by ox‑LDL, and directly targeted HMGB1 to regulate the PI3k/Akt signaling pathway. In conclusion, miR‑129‑5p inhibited the PI3k/Akt signaling pathway by directly targeting HMGB1, and reduced the viability, viability and migration of A7r5 cells induced by ox‑LDL.