Articles producció científica> Bioquímica i Biotecnologia

Role of JNK isoforms in the kainic acid experimental model of epilepsy and neurodegeneration

  • Dades identificatives

    Identificador: imarina:5131075
    Autors:
    Auladell Cde Lemos LVerdaguer EEttcheto MBusquets OLazarowski ABeas-Zarate COlloquequi JFolch JCamins A
    Resum:
    Chemoconvulsants that induce status epilepticus in rodents have been widely used over the past decades due to their capacity to reproduce with high similarity neuropathological and electroencephalographic features observed in patients with temporal lobe epilepsy (TLE). Kainic acid is one of the most used chemoconvulsants in experimental models. KA administration mainly induces neuronal loss in the hippocampus. We focused the present review inthe c-Jun N-terminal kinase-signaling pathway (JNK), since it has been shown to play a key role in the process of neuronal death following KA activation. Among the three isoforms of JNK (JNK1, JNK2, JNK3), JNK3 is widely localized in the majority of areas of the hippocampus, whereas JNK1 levels are located exclusively in the CA3 and CA4 areas and in dentate gyrus. Disruption of the gene encoding JNK3 in mice renders neuroprotection to KA, since these animals showed a reduction in seizure activity and a diminution in hippocampal neuronal apoptosis. In light of this, JNK3 could be a promising subcellular target for future therapeutic interventions in epilepsy.
  • Altres:

    Autor segons l'article: Auladell C; de Lemos L; Verdaguer E; Ettcheto M; Busquets O; Lazarowski A; Beas-Zarate C; Olloquequi J; Folch J; Camins A
    Departament: Bioquímica i Biotecnologia
    Autor/s de la URV: Folch Lopez, Jaume
    Paraules clau: Review Neuroprotection Kainic acid Hippocampus Energy metabolism C-jun n-terminal kinase signaling pathway Apoptosis Amyloid beta protein
    Resum: Chemoconvulsants that induce status epilepticus in rodents have been widely used over the past decades due to their capacity to reproduce with high similarity neuropathological and electroencephalographic features observed in patients with temporal lobe epilepsy (TLE). Kainic acid is one of the most used chemoconvulsants in experimental models. KA administration mainly induces neuronal loss in the hippocampus. We focused the present review inthe c-Jun N-terminal kinase-signaling pathway (JNK), since it has been shown to play a key role in the process of neuronal death following KA activation. Among the three isoforms of JNK (JNK1, JNK2, JNK3), JNK3 is widely localized in the majority of areas of the hippocampus, whereas JNK1 levels are located exclusively in the CA3 and CA4 areas and in dentate gyrus. Disruption of the gene encoding JNK3 in mice renders neuroprotection to KA, since these animals showed a reduction in seizure activity and a diminution in hippocampal neuronal apoptosis. In light of this, JNK3 could be a promising subcellular target for future therapeutic interventions in epilepsy.
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 10934715
    Adreça de correu electrònic de l'autor: jaume.folch@urv.cat
    Identificador de l'autor: 0000-0002-5051-8858
    Data d'alta del registre: 2023-03-05
    Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
    Enllaç font original: https://europepmc.org/article/med/27814647
    Referència a l'article segons font original: Front Biosci (Landmark Ed). 22 (5): 795-814
    Referència de l'ítem segons les normes APA: Auladell C; de Lemos L; Verdaguer E; Ettcheto M; Busquets O; Lazarowski A; Beas-Zarate C; Olloquequi J; Folch J; Camins A (2017). Role of JNK isoforms in the kainic acid experimental model of epilepsy and neurodegeneration. Front Biosci (Landmark Ed), 22(5), 795-814. DOI: 10.2741/4517
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    DOI de l'article: 10.2741/4517
    Entitat: Universitat Rovira i Virgili
    Any de publicació de la revista: 2017
    Tipus de publicació: Journal Publications
  • Paraules clau:

    Review
    Neuroprotection
    Kainic acid
    Hippocampus
    Energy metabolism
    C-jun n-terminal kinase signaling pathway
    Apoptosis
    Amyloid beta protein
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