| Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke. | |
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MedLine Citation:
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PMID: 20955426 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Stroke induces a complex web of pathophysiology that may evolve over hours to days and weeks after onset. It is now recognized that inflammation is an important phenomenon that can dramatically influence outcomes after stroke. In this minireview, we explore the hypothesis that inflammatory signals after stroke are biphasic in nature. The high-mobility group box 1 (HMGB1) protein is discussed as an example of this idea. HMGB1 is normally present in the nucleus. Under ischemic conditions, it is released extracellularly from many types of cells. During the acute phase poststroke, HMGB1 promotes necrosis and influx of damaging inflammatory cells. However, during the delayed phase poststroke, HMGB1 can mediate beneficial plasticity and recovery in many cells of the neurovascular unit. These emerging findings support the hypothesis that inflammation after stroke can be both detrimental and beneficial, depending on the cellular situations involved. |
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Authors:
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Kazuhide Hayakawa; Jianhua Qiu; Eng H Lo |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Annals of the New York Academy of Sciences Volume: 1207 ISSN: 1749-6632 ISO Abbreviation: Ann. N. Y. Acad. Sci. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-10-19 Completed Date: 2010-11-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7506858 Medline TA: Ann N Y Acad Sci Country: United States |
Other Details:
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Languages: eng Pagination: 50-7 Citation Subset: IM |
Copyright Information:
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© 2010 New York Academy of Sciences. |
Affiliation:
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Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA. khayakawa1@partners.org |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Extracellular Space / physiology HMGB1 Protein / physiology* Humans Inflammation / physiopathology* Models, Neurological Receptors, Immunologic / physiology Signal Transduction / physiology Stroke / physiopathology* Toll-Like Receptor 4 / physiology |
| Chemical | |
Reg. No./Substance:
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0/HMGB1 Protein; 0/Receptors, Immunologic; 0/Toll-Like Receptor 4; 0/advanced glycosylation end-product receptor |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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