Activation of c-Jun in the nuclei of neurons of the CA-1 in thrombin preconditioning occurs via PAR-1.

Détails

ID Serval
serval:BIB_69FED5F870C3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Activation of c-Jun in the nuclei of neurons of the CA-1 in thrombin preconditioning occurs via PAR-1.
Périodique
Journal of Neuroscience Research
Auteur⸱e⸱s
Price Melanie, Badaut Jerome, Thevenet Jonathan, Hirt Lorenz
ISSN
1097-4547[electronic], 0360-4012[linking]
Statut éditorial
Publié
Date de publication
2010
Volume
88
Numéro
6
Pages
1338-1347
Langue
anglais
Notes
BIB_98180C29158D
Résumé
Recently it has been shown that the c-Jun N-terminal kinase (JNK) plays a role in thrombin preconditioning (TPC) in vivo and in vitro. To investigate further the pathways involved in TPC, we performed an immunohistochemical study in hippocampal slice cultures. Here we show that the major target of JNK, the AP-1 transcription factor c-Jun, is activated by phosphorylation in the nuclei of neurons of the CA1 region by using phospho-specific antibodies against the two JNK phosphorylation sites. The activation is early and transient, peaking at 90 min and not present by 3 hr after low-dose thrombin administration. Treatment of cultures with a synthetic thrombin receptor agonist results in the same c-Jun activation profile and protection against subsequent OGD, both of which are prevented by specific JNK inhibitors, showing that thrombin signals through PAR-1 to JNK. By using an antibody against the Ser 73 phosphorylation site of c-Jun, we identify possible additional TPC substrates.
Mots-clé
Phospho-C-Jun Ser 63 and 73 Activation, PAR-1, Organotypic Hippocampal Slice Cultures, Thrombin Preconditioning, N-Terminal Kinase, Transcription Factor, Ischemic Tolerance, Cerebral-Ischemia, Induced Apoptosis, Brain, Expression, Pathway, AP-1, Death
Pubmed
Web of science
Open Access
Oui
Création de la notice
15/06/2011 11:01
Dernière modification de la notice
20/08/2019 14:24
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