Source:http://linkedlifedata.com/resource/pubmed/id/16899075
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2006-9-1
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pubmed:abstractText |
CCAAT/enhancer binding protein beta (C/EBPbeta) is a leucine-zipper transcription factor that regulates cell growth and differentiation in mammals. Expression of many pro-inflammatory genes including the cytokine interleukin-6 is known to be controlled by C/EBPbeta. We report that focal cerebral ischemia induced by transient middle cerebral artery occlusion (MCAO) significantly increases C/EBPbeta gene expression in mouse brain at between 6 and 72 h of reperfusion. To understand the functional significance of C/EBPbeta in postischemic inflammation and brain damage, we induced transient MCAO in cohorts of adult C/EBPbeta null mice and their wild-type littermates. At 3 days of reperfusion following transient MCAO, C/EBPbeta null mice showed significantly smaller infarcts, reduced neurological deficits, decreased terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells, decreased intercellular adhesion molecule 1 (ICAM1) immunopositive vessels, decreased extravasated neutrophils and fewer activated microglia/macrophages, compared with their wild-type littermates. Furthermore, GeneChip analysis showed that postischemic induction of many transcripts known to promote inflammation and neuronal damage was less pronounced in the brains of C/EBPbeta-/- mice compared with C/EBPbeta+/+ mice. These results suggest a significant role for C/EBPbeta in postischemic inflammation and brain damage.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Protein-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-3042
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
98
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1718-31
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16899075-Animals,
pubmed-meshheading:16899075-Apoptosis,
pubmed-meshheading:16899075-Brain,
pubmed-meshheading:16899075-CCAAT-Enhancer-Binding Protein-beta,
pubmed-meshheading:16899075-Cerebral Infarction,
pubmed-meshheading:16899075-Encephalitis,
pubmed-meshheading:16899075-Gene Expression,
pubmed-meshheading:16899075-In Situ Nick-End Labeling,
pubmed-meshheading:16899075-Intercellular Adhesion Molecule-1,
pubmed-meshheading:16899075-Interleukin-6,
pubmed-meshheading:16899075-Ischemic Attack, Transient,
pubmed-meshheading:16899075-Mice,
pubmed-meshheading:16899075-Mice, Knockout,
pubmed-meshheading:16899075-Nervous System Diseases,
pubmed-meshheading:16899075-Neurons,
pubmed-meshheading:16899075-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:16899075-RNA, Messenger,
pubmed-meshheading:16899075-Transcription, Genetic
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pubmed:year |
2006
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pubmed:articleTitle |
Decreased brain damage and curtailed inflammation in transcription factor CCAAT/enhancer binding protein beta knockout mice following transient focal cerebral ischemia.
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pubmed:affiliation |
Department of Neurological Surgery, Universit of Wisconsin, Madison, Wisconsin, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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