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Published on: May 4, 2021
miRNA-133a attenuates lipid accumulation via TR4-CD36 pathway in macrophages
Xiao-Ping Peng1, Lei Huang2, Zhi-Hong Liu1
1Department of Cardiovascular Medicine, First Affiliated Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan 412000, China.
Abstract:
lipid metabolism is the major causes of atherosclerosis. There is increasing evidence that miR-133a plays an important role in atherosclerosis. However, the regulatory mechanism of miR-133a in macrophages is still unclear. Several lines of evidence indicate that loss of TR4 leads to reduce lipid accumulation in liver and adipose tissues, etc, and lesional macrophages-derived TR4 can greatly increase the foam cell formation through increasing the CD36-mediated the uptake of ox-LDL. Interestingly, computational analysis suggests that TR4 may be a target gene of miR-133a. Here, we examined whether miR-133a regulates TR4 expression in ox-LDL-induced mouse RAW 264.7 macrophages, thereby affecting lipid accumulation. Using ox-LDL-treatment RAW 264.7 macrophages transfected with miR-133a mimics or inhibitors, we have showed that miR-133a can directly regulate the expression of TR4 in RAW 264.7 cells, thereby attenuates CD36-medide lipid accumulation. Furthermore, our studies suggest an additional explanation for the regulatory mechanism of miR-133a regulation to its functional target, TR4 in RAW 264.7 macrophages. Thus, our findings suggest that miR-133a may regulate lipid accumulation in ox-LDL-stimulated RAW 264.7 macrophages via TR4-CD36 pathway.
Insights
MicroRNA-133a (miR-133a) regulates lipid accumulation in macrophages by targeting TR4, a key factor in atherosclerosis development. This finding clarifies miR-133a's role in foam cell formation.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cell Biology
Background:
- Lipid metabolism dysregulation is a primary driver of atherosclerosis.
- MicroRNA-133a (miR-133a) is implicated in atherosclerosis, but its precise mechanism in macrophages remains elusive.
- TR4 nuclear receptor influences lipid accumulation and foam cell formation via CD36-mediated uptake of oxidized low-density lipoprotein (ox-LDL).
Purpose of the Study:
- To investigate the regulatory role of miR-133a on TR4 expression in macrophages.
- To determine if miR-133a affects lipid accumulation through the TR4-CD36 pathway in ox-LDL-stimulated macrophages.
Main Methods:
- Utilized ox-LDL-treated mouse RAW 264.7 macrophages.
- Transfected cells with miR-133a mimics and inhibitors to modulate miR-133a levels.
- Assessed TR4 expression and CD36-mediated lipid accumulation.
Main Results:
- miR-133a directly regulates TR4 expression in RAW 264.7 macrophages.
- miR-133a transfection attenuated CD36-mediated lipid accumulation.
- TR4 acts as a functional target of miR-133a in regulating lipid metabolism.
Conclusions:
- miR-133a plays a protective role against lipid accumulation in macrophages.
- The miR-133a-TR4-CD36 axis is a novel regulatory pathway influencing atherosclerosis progression.
- Targeting miR-133a may offer a therapeutic strategy for atherosclerosis.
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