Linked Life Data

16899075

Source:http://linkedlifedata.com/resource/pubmed/id/16899075

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pubmed-article:16899075pubmed:abstractTextCCAAT/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.lld:pubmed
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pubmed-article:16899075pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:16899075pubmed:articleTitleDecreased brain damage and curtailed inflammation in transcription factor CCAAT/enhancer binding protein beta knockout mice following transient focal cerebral ischemia.lld:pubmed
pubmed-article:16899075pubmed:affiliationDepartment of Neurological Surgery, Universit of Wisconsin, Madison, Wisconsin, USA.lld:pubmed
pubmed-article:16899075pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16899075pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:16899075pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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