Abstract
Although accumulating evidence indicates that cAMP response element binding protein (CREB) phosphorylation is upregulated after cerebral ischemia, it remains uncertain whether CREB phosphorylation induced after ischemia leads to CRE-mediated gene transcription and is involved in cell survival or not. Using CRE-LacZ transgenic mice, we demonstrated that CRE-mediated gene expression was found in a subset of pCREB-positive neurons after transient global and focal cerebral ischemia and in cultured neurons after exposure to glutamate. Treatment with CRE-decoy oligonucleotide suppressed upregulation of BCL-2 expression and accelerated neuronal damage after exposure to glutamate. CRE-mediated gene expression occurs in neurons after metabolic stresses and exerts its neuroprotective action through production of survival-promoting molecules such as anti-apoptotic protein BCL-2.
Published Version
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