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J Cell Physiol ; 233(10): 6630-6637, 2018 10.
Article in English | MEDLINE | ID: mdl-29226948

ABSTRACT

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.


Subject(s)
Atherosclerosis/genetics , MicroRNAs/genetics , Oxidative Stress/genetics , Toll-Like Receptor 4/genetics , Animals , Apoptosis/genetics , Atherosclerosis/pathology , CD36 Antigens/genetics , Gene Expression Regulation/genetics , Humans , Inflammation/genetics , Inflammation/pathology , Lipoproteins, LDL/genetics , Lipoproteins, LDL/metabolism , Mice , RAW 264.7 Cells , Signal Transduction/genetics
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