• Am. J. Med. Sci. · Jun 2022

    LncRNA OIP5-AS1 Promotes the Proliferation and Migration of Vascular Smooth Muscle Cells via Regulating miR-141-3p/HMGB1 Pathway.

    • Hang Dong, Guangyu Jiang, Jiayue Zhang, and Yuming Kang.
    • Department of Physiology & Pathophysiology of Xi'an Jiaotong University School of Basic Medical Sciences, Xi'an 710061, Shaanxi, China; Department of Hematology, Shenzhen Yantian District People's Hospital (Group)/Shenzhen Seventh People's Hospital, Shenzhen 518081, Guangdong, China.
    • Am. J. Med. Sci. 2022 Jun 1; 363 (6): 538-547.

    BackgroundLong non-coding RNAs (lncRNAs) have been reported to play critical roles in the pathogenesis of cardiovascular diseases. However, whether lncRNA opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) regulates the pathogenesis of atherosclerosis (AS) is still unknown.MethodsHuman vascular smooth muscle cells (VSMCs) were treated with oxidized low-density lipoprotein (ox-LDL). OIP5-AS1, miR-141-3p and HMGB1 mRNA expressions were determined using quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration, and apoptosis of VSMCs were measured using MTT method, Transwell assay and TUNEL assay, respectively. Dual-luciferase reporter gene assay, qRT-PCR, and Western blot were conducted to investigate the interactions among OIP5-AS1, miR-141-3p and high mobility group box 1 (HMGB1).ResultsOIP5-AS1 expression was markedly increased in serum samples of AS patients and VSMCs treated with ox-LDL. OIP5-AS1 over-expression remarkably promoted proliferation, migration and inhibited apoptosis of VSMCs while miR-141-3p exerted the opposite effects. Furthermore, the binding sites between OIP5-AS1 and miR-141-3p were identified. OIP5-AS1 indirectly increased HMGB1 expression in VSMCs by targeting miR-141-3p.ConclusionsOIP5-AS1 promotes the proliferation, migration and suppresses apoptosis of VSMCs through regulating miR-141-3p/HMGB1 axis.Copyright © 2022 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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