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MicroRNA-181a Reduces Cardiomyocyte Apoptosis through Regulating Inflammation in Patients with Acute Myocardial Infarction
Authors:  Fujiang Cui, M.M., Guoai Yang, M.M., Kangkang Xu, M.M., and Xue Han, B.S.
  Objective: Circulating miR-181a was considered to be a potential novel biomarker for diagnosis of acute myocardial infarction (AMI), but we know nothing about the role of miR-181a in AMI.
Study Design:
Real-time fluorescence quantitative polymerase chain reaction was used to detect miRNA or mRNA expression. ELISA assay was used to measure serological index, and western blot was used to measure protein expression.
Serum miR-181a in AMI patients was not only significantly higher than that in unstable angina (UA) patients and healthy people but had a positive correlation with serum CK-MB and cTnI but had a negative correlation with IL-6, CRP, TNF-α, and IL-1β. In THP-1 cells, miR-181a was targeted to suppress the NF-κB pathway by promoting the expression of SIRT1. In peripheral blood mononuclear cells (PBMCs) of AMI patients, the serum miR-181a was positively correlated with the expression of SIRT1 mRNA but negatively correlated with p65 mRNA. In PBMCs of healthy people, overexpression of miR-181a by transferring miR-181a–mimic could increase the expression of SIRT1.
These findings demonstrated that miR-181a regulated NF-κB–mediated PBMC inflammation by targeting SIRT1, and promotion of miR-181a expression might provide a new target for anti-inflammatory therapy for AMI.
Keywords:  acute myocardial infarction, inflammation, miR-181a, SIRT1
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