Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke
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 a...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2010-10, Vol.1207 (1), p.50-57 |
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| creator | Hayakawa, Kazuhide Qiu, Jianhua Lo, Eng H. |
| description | 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. |
| doi_str_mv | 10.1111/j.1749-6632.2010.05728.x |
| format | Article |
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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.</description><subject>Animals</subject><subject>Cellular</subject><subject>Damage</subject><subject>Extracellular Space - physiology</subject><subject>HMGB1</subject><subject>HMGB1 Protein - physiology</subject><subject>Humans</subject><subject>inflammation</subject><subject>Inflammation - physiopathology</subject><subject>Models, Neurological</subject><subject>Nuclei</subject><subject>Plasticity</subject><subject>Proteins</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - physiology</subject><subject>Recovery</subject><subject>Signal Transduction - physiology</subject><subject>stroke</subject><subject>Stroke - physiopathology</subject><subject>stroke recovery</subject><subject>Strokes</subject><subject>Toll-Like Receptor 4 - physiology</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV1v0zAUhi0EYmXwF5AlLrhK528nN0jbBO2krYD4EldHTuJ07pK4s9PR_nscOsrHDViWbPm855HP-yKEKZnStE5WU6pFkSnF2ZSR9EqkZvl0-wBNDoWHaEKI1lleMH6EnsS4IoSyXOjH6IiRQkrB1ARdnbn1tYmuwqYanO8j9g2eX83OKI5u2ZvW9Uvs-rSb1nSdGTXY9DUOtvJ3NuywaQYbcByCv7FP0aPGtNE-uz-P0ac3rz-ez7PLt7OL89PLrFI8zzOuLaGlKGzVFKKmtRVWkkbUgumGk7KsLbGsEqohWqRxKsqY5EIRSw0VSpT8GL3ac9ebsrN1ZfshmBbWwXUm7MAbB39WencNS38HXBMptUyAl_eA4G83Ng7QuVjZtjW99ZsIOadU5JLrfyq1LDjjKmdJ-eIv5cpvQrIwAk1ui0KxYuTle1UVfIzBNodfUwJjuLCCMUMYM4QxXPgRLmxT6_Pfpz40_kzzly3fXGt3_w2GxdfTD-M1AbI9wMXBbg8AE25Aaa4lfFnMYME_v5-_Yww0_w4XLMGm</recordid><startdate>201010</startdate><enddate>201010</enddate><creator>Hayakawa, Kazuhide</creator><creator>Qiu, Jianhua</creator><creator>Lo, Eng H.</creator><general>Blackwell Publishing Inc</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope><scope>7SP</scope><scope>7U5</scope><scope>L7M</scope><scope>5PM</scope></search><sort><creationdate>201010</creationdate><title>Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke</title><author>Hayakawa, Kazuhide ; 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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. 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| subjects | Animals Cellular Damage Extracellular Space - physiology HMGB1 HMGB1 Protein - physiology Humans inflammation Inflammation - physiopathology Models, Neurological Nuclei Plasticity Proteins Receptor for Advanced Glycation End Products Receptors, Immunologic - physiology Recovery Signal Transduction - physiology stroke Stroke - physiopathology stroke recovery Strokes Toll-Like Receptor 4 - physiology |
| title | Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke |
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