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Published on: April 3, 2017
Downregulation of miR-145 alleviates ox-LDL-induced inflammation by targeting QKI in macrophages
Xueqiang Feng1, Fuwang Yao2, Yuqin Lang3
1Department of Vascular Intervention, Affiliated Hospital of Weifang Medical University Weifang, Shandong Province, China.
Objective:
Atherosclerosis (AS) is a chronic inflammatory disease with high mortality. miRNAs perform a vital role in its development. This study aimed to discuss the effect of miR-145 in AS occurrence and development.
Methods:
The effects of miR-145 mimics and inhibitors on IL-6, IL-1β and TNF-α expressions were assessed by qRT-PCR and ELISA. CCK-8 was applied to examine the influence of miR-145 on macrophage proliferation. The influence of miR-145 on the QKI transcriptional activity was analyzed using luciferase reporter gene assy.
Results:
Overexpression of miR-145 could enhance the expression of IL-6, IL-1β, and TNF-α. Down-regulation of miR-145 could inhibit the proliferation of macrophages and the expression level of inflammatory cytokines. The effect of miR-145 inhibitor on the expression of inflammatory factors was partially reversed by interfering with the transcription of QKI with siRNA.
Conclusion:
miR-145 regulates the inflammatory response induced by macrophage activation through targeting QKI. It provides a means for AS targeted therapy.
Insights
MicroRNA-145 (miR-145) exacerbates atherosclerosis by increasing inflammatory cytokines and macrophage proliferation. Targeting miR-145 offers a potential therapeutic strategy for atherosclerosis.
Area of Science:
- Biomedical research
- Molecular biology
- Cardiovascular disease research
Background:
- Atherosclerosis (AS) is a significant cause of mortality.
- MicroRNAs (miRNAs) are implicated in AS pathogenesis.
- miR-145's role in AS requires further elucidation.
Purpose of the Study:
- To investigate the impact of miR-145 on atherosclerosis development.
- To explore the regulatory mechanisms of miR-145 in macrophage activation and inflammation.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and ELISA to measure cytokine expression (IL-6, IL-1β, TNF-α).
- Cell Counting Kit-8 (CCK-8) assay to assess macrophage proliferation.
- Luciferase reporter assay to analyze miR-145's effect on QKI transcriptional activity.
Main Results:
- Overexpression of miR-145 increased IL-6, IL-1β, and TNF-α levels.
- Down-regulation of miR-145 inhibited macrophage proliferation and inflammatory cytokine expression.
- Inhibition of miR-145 partially reversed inflammatory factor expression by targeting QKI.
Conclusions:
- miR-145 regulates macrophage-induced inflammatory responses by targeting QKI.
- Modulating miR-145 presents a potential therapeutic avenue for atherosclerosis.
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