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Previous Article | Next Article
The Journal of Neuroscience, October 1, 2001, 21(19):7439-7446
Differential Expression of Apoptotic Protease-Activating Factor-1 and Caspase-3 Genes and Susceptibility to Apoptosis during Brain Development and after Traumatic Brain Injury
Alexander G. Yakovlev1, Katsuya Ota2, Geping Wang1, Vilen Movsesyan1, Wei-Li Bao1, Koichiro Yoshihara2, and Alan I. Faden1 1 Department of Neuroscience, Georgetown University, Washington, DC 20007, and 2 Department of Biochemistry, Nara Medical University, Kashihara, Nara 634-8521, Japan
Neuronal apoptosis plays an essential role in early brain development and contributes to secondary neuronal loss after acute brain injury. Recent studies have provided evidence that neuronal susceptibility to apoptosis induced by traumatic or ischemic injury decreases during brain development. However, the molecular mechanisms responsible for this age-dependent phenomenon remain unclear. Here we demonstrate that, during brain maturation, the potential of the intrinsic apoptotic pathway is progressively reduced and that such repression is associated with downregulation of apoptotic protease-activating factor-1 (Apaf-1) and caspase-3 gene expression. A similar decline in apoptotic susceptibility associated with downregulation of Apaf-1 expression as a function of developmental age was also found in cultured primary rat cortical neurons. Injury-induced cytochrome c-specific cleavage of caspase-9 followed by activation of caspase-3 in mature brain correlated with marked increases in Apaf-1 and caspase-3 mRNA and protein expression. These results suggest that differential expression of Apaf-1 and caspase-3 genes may underlie regulation of apoptotic susceptibility during brain development, as well as after acute injury to mature brain, through the intrinsic pathway of caspase activation.
Key words: brain; development; injury; apoptosis; caspase; gene expression; Apaf-1
Copyright © 2001 Society for Neuroscience 0270-6474/01/21197439-08$05.00/0
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