| Heat acclimation provides sustained improvement in functional recovery and attenuates apoptosis after traumatic brain injury. | |
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MedLine Citation:
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PMID: 19904288 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Heat acclimation (HA) offers functional neuroprotection in mice after traumatic brain injury (TBI). This study further characterizes endogenous neuroprotection acquired by HA (34+/-1 degrees C, 30 d) after TBI. We establish here the ability of HA to induce sustained functional benefits and to reduce activation of apoptotic pathways. Neurobehavioral recovery, assessed by the Neurological Severity Score, was greater in HA mice up to 8 days after injury as compared with normothermic controls (P<0.05) and lesion volume was also smaller in the HA group (P<0.05). Reduced apoptotic cell death in HA mice was confirmed using caspase-3 activity measurements and immunohistochemistry. To investigate the underlying molecular pathways, expression levels of intrinsic apoptotic pathway-related proteins were examined. HA mice displayed higher mitochondrial levels of antiapoptotic Bcl-xL, accompanied by lower proapoptotic Bad levels and decreased cytochrome c release, suggesting a higher apoptotic threshold. Taken together with our previous reports, indicating increased Akt phosphorylation and antioxidative capacity, alongside with reduced tumor necrosis alpha levels after TBI in HA animals, the current results support the involvement of an antiapoptotic effect in HA-induced neuroprotection. Current results warrant further study as TBI-induced apoptosis may persist over weeks after injury, possibly providing a target for belated therapeutic intervention. |
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Authors:
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Gali Umschwief; Na'ama A Shein; Alexander G Alexandrovich; Victoria Trembovler; Michal Horowitz; Esther Shohami |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-11-11 |
Journal Detail:
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Title: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism Volume: 30 ISSN: 1559-7016 ISO Abbreviation: J. Cereb. Blood Flow Metab. Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-03-02 Completed Date: 2010-04-02 Revised Date: 2011-07-25 |
Medline Journal Info:
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Nlm Unique ID: 8112566 Medline TA: J Cereb Blood Flow Metab Country: United States |
Other Details:
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Languages: eng Pagination: 616-27 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, The Hebrew University, Jerusalem, Israel. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acclimatization
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physiology* Animals Antioxidants / metabolism Apoptosis / physiology* Behavior, Animal / physiology Blotting, Western Brain Injuries / pathology*, physiopathology Caspase 3 / metabolism Cytochromes c / biosynthesis Heart / physiopathology Hot Temperature* In Situ Nick-End Labeling Male Mice Myocardium / metabolism, pathology Oxidative Stress / physiology Proto-Oncogene Proteins c-akt / metabolism RNA, Messenger / biosynthesis, isolation & purification Recovery of Function / physiology* Reverse Transcriptase Polymerase Chain Reaction bcl-Associated Death Protein / biosynthesis bcl-X Protein / biosynthesis |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/RNA, Messenger; 0/bcl-Associated Death Protein; 0/bcl-X Protein; 9007-43-6/Cytochromes c; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 3.4.22.-/Caspase 3 |
| Comments/Corrections | |
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