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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
15
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pubmed:dateCreated |
2002-8-1
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pubmed:abstractText |
The Rho signaling pathway regulates the cytoskeleton and motility and plays an important role in neuronal growth inhibition. Here we demonstrate that inactivation of Rho or its downstream target Rho-associated kinase (ROK) stimulated neurite growth in primary cells of cortical neurons plated on myelin or chondroitin sulfate proteoglycan substrates. Furthermore, treatment either with C3 transferase (C3) to inactivate Rho or with Y27632 to inhibit ROK was sufficient to stimulate axon regeneration and recovery of hindlimb function after spinal cord injury (SCI) in adult mice. Injured mice were treated with a single injection of Rho or Rho-associated kinase inhibitors delivered in a protein adhesive at the lesion site. Treated animals showed long-distance regeneration of anterogradely labeled corticospinal axons and increased levels of GAP-43 mRNA in the motor cortex. Behaviorally, inactivation of Rho pathway induced rapid recovery of locomotion and progressive recuperation of forelimb-hindlimb coordination. These findings provide evidence that the Rho signaling pathway is a potential target for therapeutic interventions after spinal cord injury.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/ADP Ribose Transferases,
http://linkedlifedata.com/resource/pubmed/chemical/Amides,
http://linkedlifedata.com/resource/pubmed/chemical/Botulinum Toxins,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/GAP-43 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Pyridines,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Y 27632,
http://linkedlifedata.com/resource/pubmed/chemical/exoenzyme C3, Clostridium botulinum,
http://linkedlifedata.com/resource/pubmed/chemical/rho GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/rho-Associated Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1529-2401
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6570-7
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12151536-ADP Ribose Transferases,
pubmed-meshheading:12151536-Amides,
pubmed-meshheading:12151536-Animals,
pubmed-meshheading:12151536-Axons,
pubmed-meshheading:12151536-Behavior, Animal,
pubmed-meshheading:12151536-Botulinum Toxins,
pubmed-meshheading:12151536-Cell Separation,
pubmed-meshheading:12151536-Enzyme Inhibitors,
pubmed-meshheading:12151536-Female,
pubmed-meshheading:12151536-GAP-43 Protein,
pubmed-meshheading:12151536-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:12151536-Mice,
pubmed-meshheading:12151536-Mice, Inbred BALB C,
pubmed-meshheading:12151536-Motor Activity,
pubmed-meshheading:12151536-Motor Cortex,
pubmed-meshheading:12151536-Nerve Regeneration,
pubmed-meshheading:12151536-Neurites,
pubmed-meshheading:12151536-Protein-Serine-Threonine Kinases,
pubmed-meshheading:12151536-Pyridines,
pubmed-meshheading:12151536-RNA, Messenger,
pubmed-meshheading:12151536-Rats,
pubmed-meshheading:12151536-Recovery of Function,
pubmed-meshheading:12151536-Signal Transduction,
pubmed-meshheading:12151536-Spinal Cord Injuries,
pubmed-meshheading:12151536-Treatment Outcome,
pubmed-meshheading:12151536-rho GTP-Binding Proteins,
pubmed-meshheading:12151536-rho-Associated Kinases
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pubmed:year |
2002
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pubmed:articleTitle |
Rho signaling pathway targeted to promote spinal cord repair.
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pubmed:affiliation |
Département de Pathologie et Biologie Cellulaire, Université de Montréal, Montréal, Québec, H3T 1J4, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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