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Updated: Jan 4, 2026
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
MiR-210-3p attenuates lipid accumulation and inflammation in atherosclerosis by repressing IGF2
Xiang-Rui Qiao1,2, Liang Wang3, Mengping Liu1,2
1Department of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Abstract:
Previous studies have shown that miR-210-3p is involved in the development and progression of atherosclerosis, but its specific mechanisms are still unclear. This study aims to reveal the mechanism of miR-210-3p and its target genes in macrophage lipid deposition and inflammatory response, and provide new ideas for the treatment of atherosclerosis. We found miR-210-3p increased sharply in the first 12 h induced by higher doses of ox-LDL in THP-1 macrophages and then gradually decreased. MiR-210-3p mimic transfection inhibited lipid uptake and inflammatory cytokine production in ox-LDL-induced macrophages. By inhibiting IGF2/IGF2R, miR-210-3p suppressed the expression of fatty acid transcriptase CD36 and transcription factor NF-κB in ox-LDL-induced macrophages. In conclusion, miR-210-3p inhibits the expression of CD36 and NF-κB by inhibiting IGF2 / IGF2R, thereby reducing lipid accumulation and inflammatory response in ox-LDL-induced macrophages. Enhancing miR-210-3p expression may be a new strategy for the treatment of atherosclerosis.
Insights
MicroRNA-210-3p (miR-210-3p) reduces atherosclerosis by inhibiting lipid accumulation and inflammation. Enhancing miR-210-3p may offer a novel therapeutic strategy for treating this cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- MicroRNA Research
Background:
- Atherosclerosis is a complex cardiovascular disease driven by lipid deposition and inflammation in macrophages.
- The precise molecular mechanisms of microRNA-210-3p (miR-210-3p) in atherosclerosis remain incompletely understood.
Purpose of the Study:
- To elucidate the role and mechanism of miR-210-3p in regulating macrophage lipid deposition and inflammatory responses.
- To explore miR-210-3p as a potential therapeutic target for atherosclerosis.
Main Methods:
- THP-1 macrophages were treated with oxidized low-density lipoprotein (ox-LDL) to induce cellular changes.
- miR-210-3p mimic transfection was employed to assess its functional impact.
- Expression levels of key genes, including CD36 and NF-κB, were analyzed.
Main Results:
- miR-210-3p expression significantly increased in ox-LDL-treated macrophages within the initial 12 hours.
- miR-210-3p mimic transfection attenuated lipid uptake and inflammatory cytokine production.
- miR-210-3p was found to inhibit the expression of IGF2/IGF2R, subsequently suppressing CD36 and NF-κB.
Conclusions:
- miR-210-3p plays a protective role in atherosclerosis by inhibiting macrophage lipid deposition and inflammation.
- The mechanism involves the suppression of IGF2/IGF2R, leading to reduced CD36 and NF-κB expression.
- Augmenting miR-210-3p levels presents a promising therapeutic avenue for atherosclerosis treatment.
