| Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury. | |
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MedLine Citation:
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PMID: 15350969 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neonatal hypoxia-ischemia (HI) upregulates Fas death receptor expression in the brain, and alterations in expression and activity of Fas signaling intermediates occur in neonatal brain injury. B6.MRL-Tnfrsf6(lpr) mice lacking functional Fas death receptors are protected from HI brain damage in cortex, striatum, and thalamus compared to wild-type mice. Expression of Fas death receptor and active caspases increase in the cortex after HI. In wild-type mice, the hippocampus is most severely injured, and the hippocampus is the only region not protected in the B6.MRL-Tnfrsf6(lpr) mice. The selective vulnerability of the hippocampus to injury correlates with (1) lower basal expression of [Fas-associated death-domain-like IL-1beta-converting enzyme]-inhibitory protein (FLIP), (2) increased degradation of spectrin to its 145 or 150 kDa breakdown product, and (3) a higher percentage of non-apoptotic cell death following neonatal HI. We conclude that Fas signaling via both extrinsic and intrinsic caspase cascades causes brain injury following neonatal HI in a region-dependent manner. Basal levels of endogenous decoy proteins may modulate the response to Fas death receptor signaling and provide a novel approach to understanding mechanisms of neonatal brain injury. |
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Authors:
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Ernest M Graham; R Ann Sheldon; Debra L Flock; Donna M Ferriero; Lee J Martin; Declan P O'Riordan; Frances J Northington |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Neurobiology of disease Volume: 17 ISSN: 0969-9961 ISO Abbreviation: Neurobiol. Dis. Publication Date: 2004 Oct |
Date Detail:
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Created Date: 2004-09-07 Completed Date: 2004-12-21 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9500169 Medline TA: Neurobiol Dis Country: United States |
Other Details:
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Languages: eng Pagination: 89-98 Citation Subset: IM |
Affiliation:
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Department of Gyn-Ob, Division of Maternal-Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Animals, Newborn / genetics* Antigens, CD95 / biosynthesis*, genetics*, physiology Brain / metabolism*, pathology Hypoxia-Ischemia, Brain / enzymology, genetics*, metabolism*, prevention & control Mice Mice, Inbred C57BL Mice, Mutant Strains Neurons / metabolism*, pathology |
| Grant Support | |
ID/Acronym/Agency:
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AG16282/AG/NIA NIH HHS; HD 39672/HD/NICHD NIH HHS; NS 35902/NS/NINDS NIH HHS; NS 45059/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD95 |
| Comments/Corrections | |
Erratum In:
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Neurobiol Dis. 2005 Jun-Jul;19(1-2):348-9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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