MiR-140a contributes to the pro-atherosclerotic phenotype of macrophages by downregulating interleukin-10

H.-X. Yang, H.-B. Jiang, L. Luo

YongZhou Vocational Technical College, Yongzhou City, Hunan Province, China. HengboJ@yeah.net

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• Pharmacology

OBJECTIVE: The dysfunction of immune cells plays important roles in promoting the progression of atherosclerosis (AS). This study aims to investigate the role of miR-140a in modulating the function of AS-associated macrophages.

PATIENTS AND METHODS: The expression of miR-140a in human monocytes was evaluated by quantitative PCR. For in vitro studies, macrophages were transfected with miR140a mimic or miR140a inhibitor, and then, stimulated with oxidized low-density lipoprotein (ox-LDL). The production of cytokines was evaluated by quantitative PCR and enzyme-linked immunosorbent assay (ELISA). Flow cytometry was used to determine the phosphorylation of Signal Transducer and Activator of Transcription 3 (STAT3).

RESULTS: MiR-140a expression was upregulated in monocytes from AS patients. MiR140a overexpression enhanced the pro-inflammatory ability of ox-LDL-stimulated human macrophages. In addition, miR140a was found to target interleukin-10 (IL-10) in macrophages, thus reducing IL-10-mediated anti-inflammatory responses.

CONCLUSIONS: MiR-140a serves as a pro-atherosclerotic microRNA by modulating the phenotypic switch of AS-associated macrophages.

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