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dc.contributor.authorde Lemos L.
dc.contributor.authorJunyent F.
dc.contributor.authorCamins A.
dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorFolch J.
dc.contributor.authorOlloquequi J.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorVerdaguer E.
dc.contributor.authorAuladell C.
dc.date.accessioned2020-09-02T22:31:01Z
dc.date.available2020-09-02T22:31:01Z
dc.date.issued2018
dc.identifier10.1007/s12035-017-0669-1
dc.identifier.citation55, 5, 4437-4452
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6682
dc.descriptionThe activation of c-Jun-N-terminal kinases (JNK) pathway has been largely associated with the pathogenesis and the neuronal death that occur in neurodegenerative diseases. Altogether, this justifies why JNKs have become a focus of screens for new therapeutic strategies. The aim of the present study was to identify the role of the different JNK isoforms (JNK1, JNK2, and JNK3) in apoptosis and inflammation after induction of brain damage. To address this aim, we induced excitotoxicity in wild-type and JNK knockout mice (jnk1−/−, jnk2−/−, and jnk3−/−) via an intraperitoneal injection of kainic acid, an agonist of glutamic-kainate-receptors, that induce status epilepticus. Each group of animals was divided into two treatments: a single intraperitoneal dose of saline solution, used as a control, and a single intraperitoneal dose (30 mg/kg) of kainic acid. Our results reported a significant decrease in neuronal degeneration in the hippocampus of jnk1−/− and jnk3−/− mice after kainic acid treatment, together with reduced or unaltered expression of several apoptotic genes compared to WT treated mice. In addition, both jnk1−/− and jnk3−/− mice exhibited a reduction in glial reactivity, as shown by the lower expression of inflammatory genes and a reduction of JNK phosphorylation. In addition, in jnk3−/−mice, the c-Jun phosphorylation was also diminished. Collectively, these findings provide compelling evidence that the absence of JNK1 or JNK3 isoforms confers neuroprotection against neuronal damage induced by KA and evidence, for the first time, the implication of JNK1 in excitotoxicity. Accordingly, JNK1 and/or JNK3 are promising targets for the prevention of cell death and inflammation during epileptogenesis. © 2017, Springer Science+Business Media, LLC.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectc-Jun N-terminal kinase
dc.subjectExcitotoxicity
dc.subjectHippocampus
dc.subjectInflammation
dc.subjectKainic acid
dc.subjectKnockout mice
dc.subjectNeurodegeneration
dc.subjectNeuroprotection
dc.subjectisoprotein
dc.subjectJNK1 protein
dc.subjectJNK3 protein
dc.subjectkainic acid
dc.subjectunclassified drug
dc.subjectisoenzyme
dc.subjectkainic acid
dc.subjectmitogen activated protein kinase 10
dc.subjectneuroprotective agent
dc.subjectstress activated protein kinase 1
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectapoptosis
dc.subjectArticle
dc.subjectbrain damage
dc.subjectcell death
dc.subjectcontrolled study
dc.subjectepileptic state
dc.subjectepileptogenesis
dc.subjectexcitotoxicity
dc.subjectgene expression
dc.subjectinflammation
dc.subjectknockout mouse
dc.subjectmouse
dc.subjectnerve cell degeneration
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectprotein function
dc.subjectprotein phosphorylation
dc.subjectsingle drug dose
dc.subjecttemporal lobe epilepsy
dc.subjecttreatment response
dc.subjectwild type mouse
dc.subjectanimal
dc.subjectC57BL mouse
dc.subjectdeficiency
dc.subjectenzyme activation
dc.subjectenzymology
dc.subjectgenetics
dc.subjecthippocampus
dc.subjectinflammation
dc.subjectmetabolism
dc.subjectpathology
dc.subjectphosphorylation
dc.subjecttemporal lobe epilepsy
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectEnzyme Activation
dc.subjectEpilepsy, Temporal Lobe
dc.subjectHippocampus
dc.subjectInflammation
dc.subjectIsoenzymes
dc.subjectKainic Acid
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMitogen-Activated Protein Kinase 10
dc.subjectMitogen-Activated Protein Kinase 8
dc.subjectNeuroprotective Agents
dc.subjectPhosphorylation
dc.titleNeuroprotective Effects of the Absence of JNK1 or JNK3 Isoforms on Kainic Acid-Induced Temporal Lobe Epilepsy-Like Symptoms
dc.typeArticle


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