Activation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo
- Department of Respiratory Medicine, Respiratory Research Institute, The Second Affiliated Hospital, Third Military Medical University, Chongqing 400037 (China)
- Department of Scientific Research and Education, The Affiliated Baoji Hospital, Xi'an Medical University, Baoji 721006 (China)
- Department of Thoracic Surgery, Baoji Traditional Chinese Medicine Hospital, Baoji 721001 (China)
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. - Highlights: • The expression level of PPARγ is positively correlated with that of miR-124 in patients with sepsis. • PPARγ upregulates miR-124 and in turn inhibits miR-124 target gene. • PPARγ promotes miR-124 transcription through binding to miR-124 promoter region. • Inhibition of miR-124 attenuates the PPARγ-mediated suppression of proinflammatory cytokines in vitro. • PPARγ-induced miR-124 is involved in the suppression of pro-inflammatory cytokine in vivo.
- OSTI ID:
- 22697002
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 486, Issue 3; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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