Transcriptional Regulation of Fatty Acid Translocase/CD36 Expression by CCAAT/Enhancer-binding Protein α
Copyright policy )Transcriptional Regulation of Fatty Acid Translocase/CD36 Expression by CCAAT/Enhancer-binding Protein α
Fatty acid translocase (FAT/CD36) plays an important role in facilitating long chain fatty acid transport. FAT/CD36 gene deletion protects mice from high fat diet-induced obesity. In this study we have investigated the regulatory mechanism of FAT/CD36 expression at the transcription level. FAT/CD36 expression was activated during 3T3-L1 adipocyte differentiation, and FAT/CD36 protein levels were positively correlated with CCAAT/enhancer-binding protein alpha (C/EBPalpha) and peroxisome proliferator-activated receptor gamma. However, a negative correlation was detected between FAT/CD36 and C/EBPbeta. Overexpression of C/EBPalpha or C/EBPbeta increased FAT/CD36 mRNA and protein levels in several types of cells. Restoration of C/EBPalpha or C/EBPbeta expression in C/EBPalpha- or C/EBPbeta-deficient mouse embryonic fibroblasts increased FAT/CD36 expression. However, in mouse embryonic fibroblasts C/EBPalpha was a more potent activator of FAT/CD36 expression than was C/EBPbeta. Expression of C/EBPalpha robustly increased FAT/CD36 proximal promoter-directed luciferase expression in human embryonic kidney 293 cells. A C/EBP-responsive element was identified in the FAT/CD36 promoter by using 5' and specific site mutations. The binding of C/EBPalpha in the FAT/CD36 promoter was detected by chromatin immunoprecipitation in 3T3-L1 adipocytes. These results demonstrated that C/EBPalpha regulates FAT/CD36 gene expression at the transcriptional level.
- University of Kentucky United States
- National Institute of Health Pakistan
- National Institutes of Health United States
- University of Colorado System United States
- University of Colorado Denver United States
CD36 Antigens, Mice, Knockout, Transcription, Genetic, CCAAT-Enhancer-Binding Protein-beta, Cell Differentiation, Fibroblasts, Embryo, Mammalian, Response Elements, Diet, Mice, Gene Expression Regulation, 3T3-L1 Cells, Adipocytes, CCAAT-Enhancer-Binding Protein-alpha, Animals, Humans, Point Mutation, Obesity, RNA, Messenger
CD36 Antigens, Mice, Knockout, Transcription, Genetic, CCAAT-Enhancer-Binding Protein-beta, Cell Differentiation, Fibroblasts, Embryo, Mammalian, Response Elements, Diet, Mice, Gene Expression Regulation, 3T3-L1 Cells, Adipocytes, CCAAT-Enhancer-Binding Protein-alpha, Animals, Humans, Point Mutation, Obesity, RNA, Messenger
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