Title | miRNA-133a attenuates lipid accumulation via TR4-CD36 pathway in macrophages. |
Publication Type | Journal Article |
Year of Publication | 2016 |
Authors | Peng X-P, Huang L, Liu Z-H |
Journal | Biochimie |
Volume | 127 |
Pagination | 79-85 |
Date Published | 2016 Aug |
ISSN | 1638-6183 |
Keywords | Animals, Base Sequence, CD36 Antigens, Gene Expression Regulation, Lipid Metabolism, Lipoproteins, LDL, Macrophages, Mice, MicroRNAs, Nuclear Receptor Subfamily 2, Group C, Member 2, RAW 264.7 Cells, Signal Transduction |
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. |
DOI | 10.1016/j.biochi.2016.04.012 |
Alternate Journal | Biochimie |
PubMed ID | 27109382 |
Submitted by kej2006 on June 6, 2018 - 4:11pm