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Activation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo

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... Full description

Journal Title: Biochemical and Biophysical Research Communications 06 May 2017, Vol.486(3), pp.726-731
Main Author: Wang, Dan
Other Authors: Shi, Liuyan , Xin, Wei , Xu, Jiancheng , Xu, Jing , Li, Qi , Xu, Zhi , Wang, Jianchun , Wang, Guansong , Yao, Wei , He, Binfeng , Yang, Yu , Hu, Mingdong
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2017.03.106
Link: https://www.sciencedirect.com/science/article/pii/S0006291X17305764
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recordid: elsevier_sdoi_10_1016_j_bbrc_2017_03_106
title: Activation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo
format: Article
creator:
  • Wang, Dan
  • Shi, Liuyan
  • Xin, Wei
  • Xu, Jiancheng
  • Xu, Jing
  • Li, Qi
  • Xu, Zhi
  • Wang, Jianchun
  • Wang, Guansong
  • Yao, Wei
  • He, Binfeng
  • Yang, Yu
  • Hu, Mingdong
subjects:
  • Pparγ
  • Mir-124
  • Inflammatory Cytokines
  • Inflammation
  • Biology
  • Chemistry
  • Anatomy & Physiology
ispartof: Biochemical and Biophysical Research Communications, 06 May 2017, Vol.486(3), pp.726-731
description: 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 . 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.
language: eng
source:
identifier: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2017.03.106
fulltext: fulltext
issn:
  • 0006-291X
  • 0006291X
  • 1090-2104
  • 10902104
url: Link


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titleActivation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo
creatorWang, Dan ; Shi, Liuyan ; Xin, Wei ; Xu, Jiancheng ; Xu, Jing ; Li, Qi ; Xu, Zhi ; Wang, Jianchun ; Wang, Guansong ; Yao, Wei ; He, Binfeng ; Yang, Yu ; Hu, Mingdong
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subjectPparγ ; Mir-124 ; Inflammatory Cytokines ; Inflammation ; Biology ; Chemistry ; Anatomy & Physiology
descriptionPeroxisome 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 . 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.
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titleActivation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo
description

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

. 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.

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titleActivation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo
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abstract

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

. 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.

pubElsevier Inc
doi10.1016/j.bbrc.2017.03.106
lad01Biochemical and Biophysical Research Communications
date2017-05-06