Abstract
Successful axon regeneration depends on the expression of regeneration-associated genes by axotomized neurons. Here, we demonstrate, for the first time to our knowledge, the expression of regeneration-associated genes by axotomized human CNS neurons. In situ hybridization and immunohistochemistry showed a transient induction of GAP-43 and c-jun in Clarke's nucleus neurons caudal to traumatic human spinal cord injury. These results support experimental data that nonregenerating central nervous system neurons can temporarily upregulate regeneration-associated genes, reflecting a transient regenerative capacity that fails over time.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Caspase 3
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Caspases / metabolism
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GAP-43 Protein / genetics
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GAP-43 Protein / metabolism
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Genes, jun / genetics
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Humans
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Immunohistochemistry
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In Situ Hybridization
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Nerve Regeneration*
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Neurofilament Proteins / metabolism
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Neurons / metabolism*
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Neurons / pathology
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Polymerase Chain Reaction / methods
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RNA Probes / metabolism
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RNA, Messenger / biosynthesis
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RNA, Messenger / metabolism
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Spinal Cord Injuries / metabolism
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Spinal Cord Injuries / pathology*
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Time Factors
Substances
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GAP-43 Protein
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Neurofilament Proteins
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RNA Probes
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RNA, Messenger
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CASP3 protein, human
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Caspase 3
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Caspases