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Ischemic induction of protooncogene expression in gerbil brain
M S Kindy1, J P Carney, R J Dempsey
1Department of Biochemistry, University of Kentucky, Lexington 40536-0084.
Journal of Molecular Neuroscience : MN
|January 1, 1991
Summary
Cerebral ischemia increases c-fos and c-jun protooncogene expression in gerbil brains, particularly in affected areas. This gene activation correlates with ischemia duration and may be a key factor in stroke-related cell death and recovery.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Cerebral ischemia and reperfusion trigger metabolic events leading to cell death.
- Gene expression changes during ischemia may determine cellular process mechanisms.
Purpose of the Study:
- To investigate the role of protooncogenes c-fos and c-jun in cerebral ischemia.
- To understand the correlation between ischemia duration and gene expression.
Main Methods:
- Bilateral carotid occlusion in Mongolian gerbils for 10 minutes.
- Measurement of c-fos and c-jun messenger RNA and protein levels.
- Analysis of protein complex formation and AP-1 binding.
Main Results:
- Ischemia increased c-fos and c-jun mRNA in cortex and striatum, but not brain stem or cerebellum.
- Increased protooncogene mRNA correlated with ischemia duration.
- Pentobarbital pretreatment reduced ischemic effects and c-fos mRNA increase.
- Ischemia led to increased c-fos/c-jun protein complex formation associated with AP-1 binding.
Conclusions:
- Regulated expression of c-fos and c-jun protooncogenes is implicated in ischemic cell death and recovery.
- These findings suggest a potential therapeutic target for stroke and neurodegenerative disorders.