Specific JNK Inhibition by D-JNKI1 Protects Purkinje Cells from Cell Death in Lurcher Mutant Mouse
| Autor: | Vanessa Gautheron, Hadi S. Zanjani, Jean Mariani, Mariaelena Repici, Tiziana Borsello, Isabelle Dusart |
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| Přispěvatelé: | Neurobiologie des processus adaptatifs (NPA), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), CHU Charles Foix [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU) |
| Rok vydání: | 2008 |
| Předmět: |
Male
Threonine Cerebellum Programmed cell death Cell Membrane Permeability Genotype MAP Kinase Kinase 4 Mutant Lurcher Biology Mice Mice Neurologic Mutants Purkinje Cells 03 medical and health sciences 0302 clinical medicine medicine Animals Crosses Genetic 030304 developmental biology Neurons Alanine 0303 health sciences Cell Death Kinase [SCCO.NEUR]Cognitive science/Neuroscience Glutamate receptor Cell biology medicine.anatomical_structure Amino Acid Substitution Animals Newborn Receptors Glutamate Neurology Mutation Female Neurology (clinical) Peptides 030217 neurology & neurosurgery |
| Zdroj: | The Cerebellum The Cerebellum, 2008, 7 (4), pp.534-8. ⟨10.1007/s12311-008-0070-8⟩ The Cerebellum, Springer, 2008, 7 (4), pp.534-8. ⟨10.1007/s12311-008-0070-8⟩ |
| ISSN: | 1473-4230 1473-4222 |
| Popis: | International audience; In the Lurcher mutant mouse (+/Lc), Purkinje cells (PCs) selectively die due to the mutation that converts alanine to threonine in the glutamate ionotropic receptor GRID 2, thus resulting in a constitutively leaky cation channel. This intrinsic cell death determines a target-dependent cell death of granule cells and olivary neurons and cerebellum cytoarchitecture is severely disrupted in the adult Lurcher mutant. Although the +/Lc mutant has been widely characterized, less is known about the molecules involved in +/Lc PC death. We, here, used organotypic cerebellar slice cultures from P0 mice to investigate the role of c-jun N-terminal kinase (JNK) in +/Lc PC death by using D-JNKI1 as very specific tool to inhibit its action. Our results showed that D-JNKI1 treatment increased the number of +/Lc PC at 14 DIV of 3.6-fold. Conversely, this specific JNK inhibitor cell permeable peptide did not increase PC number in +/+ treated versus untreated cultures. These results clearly indicate that JNK plays an important role in +/Lc PC mechanism of cell death. |
| Databáze: | OpenAIRE |
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