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Subcellular stress response after traumatic brain injury.

Subcellular stress response after traumatic brain injury. Research Abstract Details 

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  • Subcellular stress response after traumatic brain injury. Abstract Text:

    jessie s truettnerJessie S Truettner,bingren huBingren Hu,ofelia f alonsoOfelia F Alonso,helen m bramlettHelen M Bramlett,koichi kokameKoichi Kokame,w dalton dietrichW Dalton Dietrich,

    Traumatic brain injury (TBI) initiates a complex genetic response that may include the expression of organelle specific stress genes. We investigated the effects of brain trauma on the expression of a number of stress genes by in situ hybridization and Western blot analysis including the endoplasmic reticulum (ER) stress gene grp78, ER protein processing enzymes calnexin and protein disulphide isomerase (PDI), the mitochondrial stress gene hsp60, and the cytoplasmic stress gene hsp70. Male Sprague-Dawley rats were subjected either to sham-surgery or moderate (1.8-2.2 atm) parasagittal fluid-percussion (F-P) brain injury followed by 30 min of either normoxic or hypoxic (30-40 mm Hg) gas levels. Expression of grp78 was increased in the ipsilateral cerebral cortex and dentate gyrus beginning 4 h after trauma plus hypoxia. Similarly, mRNA encoding the mitochondrial hsp60 was induced in the ipsilateral outer cortical layers at 4-24 h after TBI plus hypoxia. Calnexin and PDI mRNAs were not significantly altered following TBI with or without secondary hypoxia. In contrast, mRNA of the cytoplasmic hsp70 was strongly induced at 4 h after brain injury in multiple brain regions within the injured hemisphere, and this expression was greatly enhanced by secondary hypoxia. Because subcellular stress gene expression may reflect where unfolded or damaged proteins are abundant, these findings suggest that abnormal proteins are localized mainly in the cytoplasm, and to a lesser degree in the ER lumen and mitochondria after brain trauma. Thus, distinct parts of the cellular machinery respond to traumatic and metabolic stresses in specific ways.

    Subcellular stress response after traumatic brain injury. Publishing Authors By Initials

    js truettnerJS Truettner,b huB Hu,of alonsoOF Alonso,hm bramlettHM Bramlett,k kokameK Kokame,wd dietrichWD Dietrich,

    For similar cells: cellular structures: subcellular fractions research abstracts see: cells: cellular structures: subcellular fractions research

    PUBMED ID PMID:

    MEDLINE DATE:

    Subcellular stress response after traumatic brain injury. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of neurotrauma

    VOLUME: 24

    Page Numbers: 599-612

    Journal Abbreviation:

    ISSN: 0897-7151

    DAY: 3

    MONTH: Apr

    YEAR: 2007

    Subcellular stress response after traumatic brain injury. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8811626

    Subcellular stress response after traumatic brain injury. Keywords Mesh Terms:

    KEYWORDS: Subcellular Fractions

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Subcellular stress response after traumatic brain injury. Information

    Substance Name: Calnexin

    Registry Number: 139873-08-8

    Grant and Affiliation Information for Subcellular stress response after traumatic brain injury.

    AFFILIATION: Department of Neurological Surgery, Neurotrauma Research Center, University of Miami Miller School of Medicine, Miami, Florida 33101, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States PHS

    GRANT: NINDS 42133

    ACRONYM:

    MEDLINETA: J Neurotrauma

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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