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Published on: April 3, 2017
MiR-140a contributes to the pro-atherosclerotic phenotype of macrophages by downregulating interleukin-10
1YongZhou Vocational Technical College, Yongzhou City, Hunan Province, China. HengboJ@yeah.net.
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.
Insights
MicroRNA-140a promotes atherosclerosis by increasing inflammation in macrophages. This microRNA targets interleukin-10, reducing its anti-inflammatory effects and worsening the condition.
Area of Science:
- Immunology
- Molecular Biology
- Cardiovascular Research
Background:
- Immune cell dysfunction is a key driver of atherosclerosis (AS) progression.
- Macrophages play a critical role in the inflammatory processes underlying AS.
Purpose of the Study:
- To investigate the role of microRNA-140a (miR-140a) in regulating the function of macrophages associated with AS.
- To determine if miR-140a influences the pro-inflammatory or anti-inflammatory responses of macrophages in the context of AS.
Main Methods:
- Quantitative PCR was used to measure miR-140a expression in human monocytes.
- Macrophages were treated with miR-140a mimics or inhibitors and stimulated with oxidized low-density lipoprotein (ox-LDL).
- Cytokine production, macrophage phenotype, and STAT3 phosphorylation were analyzed.
Main Results:
- miR-140a expression was found to be upregulated in monocytes from AS patients.
- Overexpression of miR-140a enhanced the pro-inflammatory response of macrophages stimulated by ox-LDL.
- miR-140a was identified as a direct target of interleukin-10 (IL-10), thereby suppressing IL-10-mediated anti-inflammatory actions.
Conclusions:
- miR-140a acts as a pro-atherosclerotic microRNA.
- It modulates the phenotypic switch of AS-associated macrophages, promoting a pro-inflammatory state.
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