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Journal of cellular physiology v.233 no.10, 2018년, pp.6630 - 6637  

MiR‐182‐5p inhibited oxidative stress and apoptosis triggered by oxidized low‐density lipoprotein via targeting toll‐like receptor 4

Qin, Song‐Bai (Jingzhou Hospital of Chinese Traditional Medicine, The Third Clinical Medical College,Yangtze University, Jingzhou, Hubei, China ) ; Peng, Da‐Yan (Jingzhou Hospital of Chinese Traditional Medicine, The Third Clinical Medical College,Yangtze University, Jingzhou, Hubei, China ) ; Lu, Jing‐Min (Department of Neurology, Huai'an Second People's Hospital and The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, Jiangsu, China ) ; Ke, Zun‐Ping (Department of Cardiology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China ) ;

  • 초록  

    MicroRNAs (miRNAs) exhibit various roles in multiple biological processes and abnormal expression of miR‐182‐5p has been involved in many diseases. However, the role miR‐182‐5p in Atherosclerosis (AS) remains poorly understood. In our current investigation, an AS model was established by using oxidized low‐density lipoprotein (ox‐LDL) in RAW264.7 cells. miR‐182‐5p was markedly decreased in AS model dose‐dependently and time‐dependently. Additionally, CD36, oil‐red staining levels, TC, and TG were inhibited by miR‐182‐5p mimics, meanwhile ROS levels, MDA, and cell apoptosis were also restrained with an enhancement of SOD activity. Consistently, opposite results were exhibited when miR‐182‐5p inhibitors were transfected into RAW264.7 cells. It is well known that toll‐like receptor 4 (TLR4) is responsible for many inflammation diseases. By using bioinformatics analysis, TLR4 was indicated as a potential target of miR‐182‐5p. We observed TLR4 was activated in AS models and miR‐182‐5p could repress AS progression by targeting TLR4 in vitro. In conclusion, we uncovered that miR‐182‐5p played significant roles in AS through inhibiting oxidative stress and apoptosis via inactivating TLR4 expression.


  • 주제어

    atherosclerosis .   macrophage .   miR‐182‐5p .   Ox‐LDL .   TLR4.  

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