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ID 115245
タイトル別表記
IRF7 mediates MCP-1 in adipocyte
著者
Nishiguchi, Misa Tokushima University
Ugawa, Naho Tokushima University
Ishikawa, Etsuko Tokushima University
Kawabata, Yasuyo Tokushima University
Okamoto, Saya Tokushima University
Sasaki, Waka Tokushima University
Miyatake, Yumiko Tokushima University
Sebe, Mayu Tokushima University
升本, 早枝子 Fukushima University
原田, 永勝 The University of Shimane KAKEN研究者をさがす
資料タイプ
学術雑誌論文
抄録
Hypertrophy, associated with adipocyte dysfunction, causes increased pro-inflammatory adipokine, and abnormal glucose and lipid metabolism, leading to insulin resistance and obesity-related-health problems. By combining DNA microarray and genomic data analyses to predict DNA binding motifs, we identified the transcription factor Interferon Regulatory Factor 7 (IRF7) as a possible regulator of genes related to adipocyte hypertrophy. To investigate the role of IRF7 in adipocytes, we examined gene expression patterns in 3T3-L1 cells infected with a retrovirus carrying the IRF7 gene and found that enforced IRF7 expression induced the expression of monocyte chemoattractant protein-1 (MCP-1), a key initial adipokine in the chronic inflammation of obesity. CRISPR/Cas9 mediated-suppression of IRF7 significantly reduced MCP-1 mRNA. Luciferase assays, chromatin immunoprecipitation PCR analysis and gel shift assay showed that IRF7 transactivates the MCP-1 gene by binding to its proximal Interferon Stimulation Response Element (ISRE), a putative IRF7 binding motif. IRF7 knockout mice exhibited lower expression of MCP-1 in epidydimal white adipose tissue under high-fat feeding conditions, suggesting the transcription factor is physiologically important for inducing MCP-1. Taken together, our results suggest that IRF7 transactivates MCP-1 mRNA in adipocytes, and it may be involved in the adipose tissue inflammation associated with obesity.
掲載誌名
PLOS ONE
ISSN
19326203
出版者
PLOS
15
5
開始ページ
e0233390
発行日
2020-05-21
権利情報
© 2020 Kuroda et al. This is an open access article distributed under the terms of the Creative Commons Attribution License(https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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出版社版DOI
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フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系