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Decreased brain damage and curtailed inflammation in transcription factor CCAAT/enhancer binding protein beta knockout mice following transient focal cerebral ischemia

  1. Author:
    Kapadia, R.
    Tureyen, K.
    Bowen, K. K.
    Kalluri, H.
    Johnson, P. F.
    Vemuganti, R.

  2. Author Address

    Univ Wisconsin, Dept Neurol Surg, Madison, WI 53792 USA. Univ Wisconsin, Neurosci Training Program, Madison, WI 53792 USA. Univ Wisconsin, Cardiovasc Res Ctr, Madison, WI 53792 USA. NCI, Lab Prot Dynam & Signaling, Frederick, MD 21701 USA.;Vemuganti, R, Univ Wisconsin, Dept Neurol Surg, K4-8 Mail Stop Code CSC-8660,600 Highland Ave, Madison, WI 53792 USA.;vemugant@neurosurg.wisc.edu
    1. Year: 2006
    2. Date: Sep
  2. Journal: Journal of Neurochemistry
    1. 98
    2. 6
    3. Pages: 1718-1731
  4. Type of Article: Article
  5. ISSN: 0022-3042
  1. Abstract:

    CCAAT/enhancer binding protein beta (C/EBP beta) 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/EBP beta. We report that focal cerebral ischemia induced by transient middle cerebral artery occlusion (MCAO) significantly increases C/EBP beta gene expression in mouse brain at between 6 and 72 h of reperfusion. To understand the functional significance of C/EBP beta in postischemic inflammation and brain damage, we induced transient MCAO in cohorts of adult C/EBP beta null mice and their wild-type littermates. At 3 days of reperfusion following transient MCAO, C/EBP beta 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/EBP beta-/- mice compared with C/EBP beta+/+ mice. These results suggest a significant role for C/EBP beta in postischemic inflammation and brain damage.

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External Sources

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  2. DOI: 10.1111/j.1471-4159.2006.04056.x
  3. View record in Web of Science®
  4. WOS: 000240033600003

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