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E-GEOD-16735 - Evidence for a rheostat that determines neuronal survival after traumatic brain injury

Released on 20 December 2010
Rattus norvegicus
Samples (8)
Array (1)
Protocols (7)
To investigate the determinants of neuronal survival after traumatic brain injury, we compared the transcriptional profiles of dying (Fluoro-Jade-positive) and immediately adjacent surviving (Fluoro-Jade-negative) neurons from the CA3 subfield of the rat hippocampus 24 hours after experimental TBI. We found that hippocampal neurons that survive TBI invariably express high levels of genes that have cellular functions involved in survival, regeneration, development, proliferation, neuronal plasticity such as cAMP response element binding protein (CREB), brain-derived-neurotrophic factor (BDNF) and mitogen-activated protein kinase 1 (MAPK1). Dying neurons express high levels of genes involved in aberrant cell cycle progression, immune response, inflammation, oxidative stress and apoptosis such as Interleukin-1β (IL-1β), caspase 3 and B-cell linker (BLNK). We conclude that shifting the balance between the global levels of these proteins with pharmacotherapeutic drugs that induce expression of cell survival associated genes, is expected to alter the cellular rheostat that determines cell survival or cell death. Replicate pooled samples (approximately 600 laser capture microdissected hippocampal neurons per sample of dying neurons (labeled with Fluoro-Jade, a fluorescent stain for degenerating CNS neurons) and surviving neurons (Fluoro-Jade-negative) were hybridized in duplicate to rat Agilent whole genome arrays.
Experiment type
transcription profiling by array 
Investigation descriptionE-GEOD-16735.idf.txt
Sample and data relationshipE-GEOD-16735.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-MEXP-784.adf.txt