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Neuronal plasticity after spinal cord injury: identification of a gene cluster driving neurite outgrowth
Author(s) -
Di Giovanni Simone,
Faden Alan I.,
Yakovlev Alexander,
Duke-Cohan Jonathan S.,
Finn Tom,
Thouin Melissa,
Knoblach Susan,
De Biase Andrea,
Bregman Barbara S.,
Hoffman Eric P.
Publication year - 2005
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.04-2694fje
Subject(s) - neurite , dorsal root ganglion , biology , spinal cord , spinal cord injury , axon , neuroscience , microbiology and biotechnology , gdf7 , myelin , oligodendrocyte , gene , central nervous system , genetics , in vitro , embryonic stem cell
Functional recovery after spinal cord injury (SCI) may result in part from axon outgrowth and related plasticity through coordinated changes at the molecular level. We employed microarray analysis to identify a subset of genes the expression patterns of which were temporally coregulated and correlated to functional recovery after SCI. Steady‐state mRNA levels of this synchronously regulated gene cluster were depressed in both ventral and dorsal horn neurons within 24 h after injury, followed by strong re‐induction during the following 2 wk, which paralleled functional recovery. The identified cluster includes neuritin, attractin, microtubule‐ associated protein 1a, and myelin oligodendrocyte protein genes. Transcriptional and protein regulation of this novel gene cluster was also evaluated in spinal cord tissue and in single neurons and was shown to play a role in axonal plasticity. Finally, in vitro transfection experiments in primary dorsal root ganglion cells showed that cluster members act synergistically to drive neurite outgrowth.

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