| EGCG stimulates autophagy and reduces cytoplasmic HMGB1 levels in endotoxin-stimulated macrophages. | |
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MedLine Citation:
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PMID: 21371444 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Historically, consumption of Green tea (Camellia sinensis) has been associated with health benefits against multiple diseases including cancer, atherosclerosis and cardiovascular disorders. Emerging evidence has suggested a pathogenic role for HMGB1, a newly identified "late" mediator of lethal systemic inflammation, in the aforementioned diseases. Here we demonstrated that a major ingredient of Green tea, EGCG, was internalized into HMGB1-containing LC3-positive cytoplasmic vesicles (likely autophagosomes) in macrophages, and induced HMGB1 aggregation in a time-dependent manner. Furthermore, EGCG stimulated LC3-II production and autophagosome formation, and inhibited LPS-induced HMGB1 up-regulation and extracellular release. The EGCG-mediated HMGB1 inhibitory effects were diminished by inhibition of class III phosphatidylinositol-3 kinase (with 3-methyladenine) or knockdown of an essential autophagy-regulating protein, beclin-1. Moreover, the EGCG-mediated protection against lethal sepsis was partly impaired by co-administration of an autophagy inhibitor, chloroquine. Taken together, the present study has suggested a possibility that EGCG inhibits HMGB1 release by stimulating its autophagic degradation. |
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Authors:
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Wei Li; Shu Zhu; Jianhua Li; Andrei Assa; Arvin Jundoria; Jianying Xu; Saijun Fan; N Tony Eissa; Kevin J Tracey; Andrew E Sama; Haichao Wang |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2011-03-01 |
Journal Detail:
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Title: Biochemical pharmacology Volume: 81 ISSN: 1873-2968 ISO Abbreviation: Biochem. Pharmacol. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-07 Completed Date: 2011-06-06 Revised Date: 2012-05-02 |
Medline Journal Info:
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Nlm Unique ID: 0101032 Medline TA: Biochem Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 1152-63 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autophagy / drug effects* Blotting, Western Catechin / analogs & derivatives*, pharmacology Cell Line Cytoplasm / drug effects*, metabolism HMGB1 Protein / metabolism* Lipopolysaccharides / pharmacology* Macrophages / drug effects*, metabolism, ultrastructure Male Mice Mice, Inbred BALB C Microscopy, Electron, Transmission RNA Interference Rats |
| Grant Support | |
ID/Acronym/Agency:
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R01 AT005076-01A2/AT/NCCAM NIH HHS; R01 AT005076-02/AT/NCCAM NIH HHS; R01 GM063075-07/GM/NIGMS NIH HHS; R01AT005076/AT/NCCAM NIH HHS; R01GM063075/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/HMGB1 Protein; 0/Lipopolysaccharides; 154-23-4/Catechin; 989-51-5/epigallocatechin gallate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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