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- Title
Decreased brain damage and curtailed inflammation in transcription factor CCAAT/enhancer binding protein β knockout mice following transient focal cerebral ischemia.
- Authors
Kapadia, Ramya; Tureyen, Kudret; Bowen, Kellie K.; Kalluri, Haviryaji; Johnson, Peter F.; Vemuganti, Raghu
- Abstract
CCAAT/enhancer binding protein β (C/EBPβ) 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/EBPβ. We report that focal cerebral ischemia induced by transient middle cerebral artery occlusion (MCAO) significantly increases C/EBPβ gene expression in mouse brain at between 6 and 72 h of reperfusion. To understand the functional significance of C/EBPβ in postischemic inflammation and brain damage, we induced transient MCAO in cohorts of adult C/EBPβ null mice and their wild-type littermates. At 3 days of reperfusion following transient MCAO, C/EBPβ 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/EBPβ–/– mice compared with C/EBPβ+/+ mice. These results suggest a significant role for C/EBPβ in postischemic inflammation and brain damage.
- Subjects
NEUROSCIENCES; INFLAMMATORY mediators; CELL death; BRAIN damage; GENE expression
- Publication
Journal of Neurochemistry, 2006, Vol 98, Issue 6, p1718
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/j.1471-4159.2006.04056.x