Document Detail


Increased susceptibility of S100B transgenic mice to perinatal hypoxia-ischemia.
MedLine Citation:
PMID:  15236402     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
S100B is a glial-derived protein that is a well-established biomarker for severity of neurological injury and prognosis for recovery. Cell-based and clinical studies have implicated S100B in the initiation and maintenance of a pathological, glial-mediated proinflammatory state in the central nervous system. However, the relationship between S100B levels and susceptibility to neurological injury in vivo has not been determined. We used S100B transgenic (Tg) and knockout (KO) mice to test the hypothesis that overexpression of S100B increases vulnerability to cerebral hypoxic-ischemic injury and that this response correlates with an increase in neuroinflammation from activated glia. Postnatal day 8 Tg mice subjected to hypoxia-ischemia showed a significant increase in mortality compared with KO and wild-type mice. Tg mice also exhibited greater cerebral injury and volume loss in the ischemic hemisphere after an 8-day recovery, as assessed by histopathology and magnetic resonance imaging. Measurement of glial fibrillary acidic protein and S100B levels showed a significant increase in the Tg mice, consistent with heightened glial activation and neuroinflammation in response to injury. This is the first demonstration to our knowledge that overexpression of S100B in vivo enhances pathological response to injury.
Authors:
Mark S Wainwright; Jeffrey M Craft; W Sue T Griffin; Alexander Marks; Jose Pineda; Kyle R Padgett; Linda J Van Eldik
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Annals of neurology     Volume:  56     ISSN:  0364-5134     ISO Abbreviation:  Ann. Neurol.     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-07-05     Completed Date:  2004-08-31     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7707449     Medline TA:  Ann Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  61-7     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Division of Neurology, Children's Memorial Hospital, Chicago, IL, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Anoxia / metabolism*,  pathology
Biological Markers
Brain / metabolism,  pathology
Brain Ischemia / metabolism*,  pathology
Genetic Predisposition to Disease
Glial Fibrillary Acidic Protein / metabolism
Humans
Magnetic Resonance Imaging
Mice
Mice, Inbred Strains
Mice, Knockout
Mice, Transgenic
Nerve Growth Factors / genetics,  metabolism*
S100 Proteins / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
KO8 NS044998/NS/NINDS NIH HHS; P01 AG12411/AG/NIA NIH HHS; P41 RR16105/RR/NCRR NIH HHS; R01 AG20243/AG/NIA NIH HHS; R01 HD37989/HD/NICHD NIH HHS; R37 AG13939/AG/NIA NIH HHS; T32 AG00260/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Glial Fibrillary Acidic Protein; 0/Nerve Growth Factors; 0/S-100 calcium-binding protein beta subunit; 0/S100 Proteins

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