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CREB and cAMP response element-mediated gene expression in the ischemic brain
1Stroke Division, Department of Neurology, Osaka University Graduate School of Medicine, Suita, Japan. kitagawa@medone.med.osaka-u.ac.jp
The FEBS Journal
|June 15, 2007
Summary
Cyclic AMP response element-binding protein (CREB) activation aids neuronal survival and neuroprotection following cerebral ischemia. Targeting CREB may offer therapeutic benefits for stroke recovery and brain protection.
Area of Science:
- Neuroscience
- Molecular Biology
- Cellular Biology
Background:
- Cerebral ischemia induces cAMP response element-binding protein (CREB) phosphorylation and CRE-mediated gene expression in neurons.
- Glutamate receptor activation and calcium influx are potential triggers for CREB activation post-ischemia.
Purpose of the Study:
- To summarize the role of CREB in regulating CRE-mediated gene expression during cerebral ischemia.
- To highlight CREB's involvement in neuroprotection, ischemic tolerance, and neurogenesis.
Main Methods:
- This review synthesizes findings from recent studies on CREB function in cerebral ischemia.
- Literature review focusing on CREB phosphorylation, gene expression, and neuronal survival.
Main Results:
- CREB activation promotes the expression of neuroprotective genes, like Bcl-2, enhancing neuronal survival post-ischemia.
- CREB is implicated in the development of ischemic tolerance and the survival of new neurons in the hippocampus.
Conclusions:
- CREB-based therapeutics show promise for brain protection, promoting neurogenesis, and improving functional recovery in stroke patients.
- Understanding CREB's role is crucial for developing novel strategies against ischemic brain injury.
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