Activation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo
Autor: | Jing Xu, Wei Xin, Yu Yang, Guansong Wang, Jiancheng Xu, Binfeng He, Mingdong Hu, Liuyan Shi, Jian-chun Wang, Qi Li, Zhi Xu, Dan Wang, Wei Yao |
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Rok vydání: | 2017 |
Předmět: |
Lipopolysaccharides
0301 basic medicine medicine.medical_treatment Biophysics Inflammation Biochemistry Cell Line Proinflammatory cytokine Mice 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation In vivo Sepsis medicine Animals Humans Promoter Regions Genetic Receptor Molecular Biology Mice Inbred BALB C Binding Sites Interleukin-6 Tumor Necrosis Factor-alpha Chemistry Macrophages Antagomirs Promoter Cell Biology Molecular biology In vitro PPAR gamma MicroRNAs 030104 developmental biology Cytokine Gene Expression Regulation Case-Control Studies 030220 oncology & carcinogenesis Cancer research medicine.symptom Protein Binding Signal Transduction |
Zdroj: | Biochemical and Biophysical Research Communications. 486:726-731 |
ISSN: | 0006-291X |
DOI: | 10.1016/j.bbrc.2017.03.106 |
Popis: | Peroxisome proliferator-activated receptor gamma (PPARγ) and miR-124 have been reported to play important roles in regulation of inflammation. However, the underlying anti-inflammatory mechanisms remain not well understood. In the present study, we demonstrated that the expression level of PPARγ is positively correlated with that of miR-124 in patients with sepsis. Activation of PPARγ upregulates miR-124 and in turn inhibits miR-124 target gene. PPARγ bound directly to PPRE in the miR-124 promoter region, and enhanced the promoter transcriptional activity. PPARγ-induced miR-124 is involved in the suppression of pro-inflammatory cytokine in vitro and in vivo. These results suggest that PPARγ-induced miR-124 inhibits the production of pro-inflammatory cytokines is a novel PPARγ anti-inflammatory mechanism and also indicate that miR-124 may be a potential therapeutic target for the treatment of inflammatory diseases. |
Databáze: | OpenAIRE |
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