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Adiponectin suppression of late inflammatory mediator, HMGB1-induced cytokine expression in RAW264 macrophage cells

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Title: Adiponectin suppression of late inflammatory mediator, HMGB1-induced cytokine expression in RAW264 macrophage cells
Authors: Elfeky, Mohamed Browse this author
Yoneshiro, Takeshi Browse this author
Okamatsu-Ogura, Yuko Browse this author →KAKEN DB
Kimura, Kazuhiro Browse this author →KAKEN DB
Keywords: adiponectin
high-mobility group protein B1
toll-like receptor 4
Issue Date: Feb-2018
Publisher: Oxford University Press
Journal Title: Journal of biochemistry
Volume: 163
Issue: 2
Start Page: 143
End Page: 153
Publisher DOI: 10.1093/jb/mvx069
PMID: 29048484
Abstract: High-mobility group protein B1 (HMGB1) is a late inflammatory mediator released from inflammatory cells when stimulated, resulting in exaggerating septic symptoms. We recently demonstrated that full-length adiponectin, a potent anti-inflammatory adipokine, inhibits lipopolysaccharide-induced HMGB1 release. However, the effects of adiponectin on HMGB1-induced exaggerating signals currently remain unknown. This study aimed to investigate the effects of adiponectin on the pro-inflammatory function of HMGB1 in RAW264 macrophage cells. The treatment of RAW264 cells with HMGB1 significantly up-regulated the mRNA expression of tumour necrosis factor-alpha, interleukin-1 beta and C-X-C motif chemokine 10. HMGB1-induced cytokine expression was markedly suppressed by a toll-like receptor 4 (TLR4) antagonist and slightly suppressed by an antagonist of the receptor for advanced glycation end products. A prior treatment with full-length or globular adiponectin dose-dependently suppressed all types of HMGB1-induced cytokine expression, and this suppression was abolished by compound C, an AMPK inhibitor, but not by the haem oxygenase (HO)-1 inhibitor, zinc protoporphyrin IX. Both forms of adiponectin also reduced the mRNA expression of TLR4. These results suggest that full-length and globular adiponectin suppress HMGB1-induced cytokine expression through an AMPK-mediated HO-1-independent pathway.
Rights: This is a pre-copyedited, author-produced version of an article accepted for publication in The journal of biochemistry following peer review. The version of record Volume 163, Issue 2, Pages 143-153, 2018 is available online at:
Type: article (author version)
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 木村 和弘

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