ID | 60237 |
フルテキストURL | |
著者 |
Gao, Shangze
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Wake, Hidenori
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Sakaguchi, Masakiyo
Department of Cell Biology,Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Wang, Dengli
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Takahashi, Youhei
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Teshigawara, Kiyoshi
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Zhong, Hui
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Mori, Shuji
Department of Pharmacology, School of Pharmacy, Shujitsu University
Liu, Keyue
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Takahashi, Hideo
Department of Pharmacology, Faculty of Medicine, Kindai University
Nishibori, Masahiro
Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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抄録 | High-mobility group box-1 (HMGB1) protein has been postulated to play a pathogenic role in severe sepsis. Histidine-rich glycoprotein (HRG), a 75 kDa plasma protein, was demonstrated to improve the survival rate of septic mice through the regulation of neutrophils and endothelium barrier function. As the relalionship of HRG and HMGB1 remains poorly understood, we investigated the effects of HRG on HMGB1-mediated pathway in endothelial cells, focusing on the involvement of specific receptors for HRG. HRC potently inhibited the HMGB1 mobilization and effectively suppressed rHMGB1-induced inflammatory responses and expression of all three HMGB1 receptors in endothelial cells. Moreover, we first clarified that these protective effects of HRG on endothelial cells were mediated through C-type lectin domain family 1 member A (CLEC-1A) receptor. Thus, current study elueiates protective effects of HRG on vascular endothelial cells through inhintion of HMGB1-mediated pathways may contribute to the therapeutic effects of HRG on severe sepsis.
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発行日 | 2020-06-26
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出版物タイトル |
iScience
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巻 | 23巻
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号 | 6号
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出版者 | Cell Press
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開始ページ | 101180
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ISSN | 2589-0042
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | © 2020 The Authors.
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.1016/j.isci.2020.101180
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ライセンス | http://creativecommons.org/licenses/by/4.0/
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助成機関名 |
Japan Agency for Medical Research and Development
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助成番号 | JP19 im0210109
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