Regulation of neuroprotective action of vasoactive intestinal peptide in the murine developing brain by protein kinase C and mitogen-activated protein kinase cascades: in vivo and in vitro studies

Détails

ID Serval
serval:BIB_1AB42C77186E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Regulation of neuroprotective action of vasoactive intestinal peptide in the murine developing brain by protein kinase C and mitogen-activated protein kinase cascades: in vivo and in vitro studies
Périodique
Journal of Neurochemistry
Auteur(s)
Gressens  P., Marret  S., Martin  J. L., Laquerriere  A., Lombet  A., Evrard  P.
ISSN
0022-3042
Statut éditorial
Publié
Date de publication
06/1998
Peer-reviewed
Oui
Volume
70
Numéro
6
Pages
2574-84
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jun
Résumé
Intracerebral administration of the excitotoxin ibotenate to newborn mice induces white matter lesions mimicking periventricular leukomalacia, the most frequent brain lesion occurring in premature human babies. In this model, coinjection of vasoactive intestinal peptide prevents white matter lesions. In the present study, coadministration of ibotenate, vasoactive intestinal peptide, and selective transduction inhibitors showed that protein kinase C and mitogen-associated protein kinase pathways were critical for neuroprotection. In vivo and in vitro immunocytochemistry revealed that vasoactive intestinal peptide activated protein kinase C in astrocytes and neurons, and mitogen-associated protein kinase in neurons. In vitro neuronal transduction activation was indirect and required medium conditioned by astrocytes in which protein kinase C had been activated by vasoactive intestinal peptide. Although vasoactive intestinal peptide did not prevent the initial in vivo appearance of white matter lesion, it promoted a secondary repair of this lesion with axonal regrowth. Through protein kinase C activation, vasoactive intestinal peptide also prevented ibotenate-induced white matter astrocyte death. These data support the following hypothetical model: Vasoactive intestinal peptide activates protein kinase C in astrocytes, which promotes astrocytic survival and release of soluble factors; these released factors activate neuronal mitogen-associated protein kinase and protein kinase C, which will permit axonal regrowth.
Mots-clé
Animals Animals, Newborn Astrocytes/drug effects/enzymology/ultrastructure Axons/drug effects/enzymology/ultrastructure Brain/*drug effects/enzymology/pathology/ultrastructure Brain Diseases/chemically induced/pathology/prevention & control Calcium-Calmodulin-Dependent Protein Kinases/*metabolism Cell Death/drug effects Cells, Cultured Cerebral Cortex/drug effects/enzymology/pathology/ultrastructure Cysts/chemically induced/pathology/prevention & control/ultrastructure Excitatory Amino Acid Agonists/toxicity Ibotenic Acid/toxicity Immunohistochemistry Mice Neurons/drug effects/enzymology/ultrastructure Neuroprotective Agents/*pharmacology Neurotoxins/toxicity Protein Kinase C/*metabolism Signal Transduction/drug effects Vasoactive Intestinal Peptide/*pharmacology
Pubmed
Web of science
Création de la notice
20/01/2008 18:22
Dernière modification de la notice
20/08/2019 12:51
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