Journal
NEUROBIOLOGY OF DISEASE
Volume 46, Issue 3, Pages 710-721Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2012.03.014
Keywords
JNK; c-jun; Caspase-3; Spinal cord injury; Neuroprotection; Locomotor recovery
Categories
Funding
- Centre National de la Recherche Scientifique (CNRS)
- Universite Pierre et Marie Curie (UPMC)
- Agence Nationale pour la Recherche [ANR-08-MNP-017]
- Institut de Recherche sur la Moelle epiniere et l'Encephale (IRME)
- Fondation pour la Recherche Medicate (FRM)
- Marie Curie Industry-Academia Partnerships and Pathways (IAPP) Cpads, San Paolo [2008-2437]
- CARIPLO [2009-2425]
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Limiting the development of secondary damage represents one of the major goals of neuroprotective therapies after spinal cord injury. Here, we demonstrate that specific JNK inhibition via a single intraperitoneal injection of the cell permeable peptide D-JNKI1 6 h after lesion improves locomotor recovery assessed by both the footprint and the BMS tests up to 4 months post-injury in mice. JNK inhibition prevents c-jun phosphorylation and caspase-3 cleavage, has neuroprotective effects and results in an increased sparing of white matter at the lesion site. Lastly, D-JNKI1 treated animals show a lower increase of erythrocyte extravasation and blood brain barrier permeability, thus indicating protection of the vascular system. In total, these results clearly point out JNK inhibition as a promising neuroprotective strategy for preventing the evolution of secondary damage after spinal cord injury. (C) 2012 Elsevier Inc. All rights reserved.
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