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Updated: Feb 27, 2026
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
miR-497 accelerates oxidized low-density lipoprotein-induced lipid accumulation in macrophages by repressing the
Junfeng Cui1, Zhong Ren2, Wenshuang Zou3
1Clinical Training Center, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, China.
Abstract:
microRNAs (miRNAs) play important roles in the pathogenesis of atherosclerosis. A previous study has reported that miR-497 is elevated in advanced atherosclerotic lesions in an apoE-deficient (apoE-/-) mouse model. The purpose of this study is to test whether miR-497 can modulate macrophage foam cell formation, an initiating event in atherosclerosis. We found that miR-497 was upregulated in THP-1 macrophages after treatment with oxidized low-density lipoprotein (oxLDL). Enforced expression of miR-497 promoted lipid accumulation and decreased cholesterol efflux in oxLDL-exposed THP-1 macrophages. In contrast, downregulation of miR-497 suppressed oxLDL-induced lipid accumulation in THP-1 macrophages. Apelin was identified to be a downstream target of miR-497. Overexpression of miR-497 significantly reduced the expression of apelin in THP-1 macrophages. Interestingly, delivery of a miR-497-resistant variant of apelin significantly inhibited lipid accumulation and enhanced cholesterol efflux in miR-497-overexpressing THP-1 macrophages in response to oxLDL. In addition, miR-497 expression was increased and negatively correlated with apelin protein expression in human atherosclerotic lesions. In conclusion, miR-497 contributes to oxLDL-induced lipid deposition in macrophages largely via targeting of apelin and thus represents a potential therapeutic target for atherosclerosis.
Insights
MicroRNAs (miRNAs) like miR-497 promote lipid buildup in macrophages, a key step in atherosclerosis development. Targeting miR-497 may offer a new therapeutic strategy for this cardiovascular disease.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiovascular Research
Background:
- MicroRNAs (miRNAs) are crucial regulators in atherosclerosis pathogenesis.
- Previous research indicated elevated miR-497 levels in advanced atherosclerotic lesions of apoE-deficient mice.
Purpose of the Study:
- To investigate the role of miR-497 in modulating macrophage foam cell formation.
- To determine if miR-497 influences lipid accumulation and cholesterol efflux in macrophages.
Main Methods:
- Utilized THP-1 macrophages treated with oxidized low-density lipoprotein (oxLDL).
- Manipulated miR-497 expression (upregulation and downregulation) and assessed its effects on lipid metabolism.
- Identified and validated apelin as a downstream target of miR-497.
- Analyzed miR-497 and apelin expression in human atherosclerotic lesions.
Main Results:
- miR-497 expression increased in THP-1 macrophages upon oxLDL treatment.
- Overexpression of miR-497 enhanced lipid accumulation and reduced cholesterol efflux.
- Downregulation of miR-497 inhibited oxLDL-induced lipid accumulation.
- miR-497 directly targeted and reduced apelin expression.
- Restoring apelin function counteracted the effects of miR-497 overexpression.
- A negative correlation between miR-497 and apelin was observed in human atherosclerotic lesions.
Conclusions:
- miR-497 promotes oxLDL-induced lipid deposition in macrophages by targeting apelin.
- miR-497 represents a potential therapeutic target for atherosclerosis.
