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Neuroprotective Effects of the Absence of JNK1 or JNK3 Isoforms on Kainic Acid-Induced Temporal Lobe Epilepsy-Like Symptoms
dc.contributor.author | de Lemos L. | |
dc.contributor.author | Junyent F. | |
dc.contributor.author | Camins A. | |
dc.contributor.author | Castro-Torres R.D. | |
dc.contributor.author | Folch J. | |
dc.contributor.author | Olloquequi J. | |
dc.contributor.author | Beas-Zarate C. | |
dc.contributor.author | Verdaguer E. | |
dc.contributor.author | Auladell C. | |
dc.date.accessioned | 2020-09-02T22:31:01Z | |
dc.date.available | 2020-09-02T22:31:01Z | |
dc.date.issued | 2018 | |
dc.identifier | 10.1007/s12035-017-0669-1 | |
dc.identifier.citation | 55, 5, 4437-4452 | |
dc.identifier.issn | 08937648 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/6682 | |
dc.description | The 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.iso | en | |
dc.publisher | Humana Press Inc. | |
dc.subject | c-Jun N-terminal kinase | |
dc.subject | Excitotoxicity | |
dc.subject | Hippocampus | |
dc.subject | Inflammation | |
dc.subject | Kainic acid | |
dc.subject | Knockout mice | |
dc.subject | Neurodegeneration | |
dc.subject | Neuroprotection | |
dc.subject | isoprotein | |
dc.subject | JNK1 protein | |
dc.subject | JNK3 protein | |
dc.subject | kainic acid | |
dc.subject | unclassified drug | |
dc.subject | isoenzyme | |
dc.subject | kainic acid | |
dc.subject | mitogen activated protein kinase 10 | |
dc.subject | neuroprotective agent | |
dc.subject | stress activated protein kinase 1 | |
dc.subject | animal cell | |
dc.subject | animal experiment | |
dc.subject | animal tissue | |
dc.subject | apoptosis | |
dc.subject | Article | |
dc.subject | brain damage | |
dc.subject | cell death | |
dc.subject | controlled study | |
dc.subject | epileptic state | |
dc.subject | epileptogenesis | |
dc.subject | excitotoxicity | |
dc.subject | gene expression | |
dc.subject | inflammation | |
dc.subject | knockout mouse | |
dc.subject | mouse | |
dc.subject | nerve cell degeneration | |
dc.subject | neuroprotection | |
dc.subject | nonhuman | |
dc.subject | protein function | |
dc.subject | protein phosphorylation | |
dc.subject | single drug dose | |
dc.subject | temporal lobe epilepsy | |
dc.subject | treatment response | |
dc.subject | wild type mouse | |
dc.subject | animal | |
dc.subject | C57BL mouse | |
dc.subject | deficiency | |
dc.subject | enzyme activation | |
dc.subject | enzymology | |
dc.subject | genetics | |
dc.subject | hippocampus | |
dc.subject | inflammation | |
dc.subject | metabolism | |
dc.subject | pathology | |
dc.subject | phosphorylation | |
dc.subject | temporal lobe epilepsy | |
dc.subject | Animals | |
dc.subject | Apoptosis | |
dc.subject | Enzyme Activation | |
dc.subject | Epilepsy, Temporal Lobe | |
dc.subject | Hippocampus | |
dc.subject | Inflammation | |
dc.subject | Isoenzymes | |
dc.subject | Kainic Acid | |
dc.subject | Mice, Inbred C57BL | |
dc.subject | Mice, Knockout | |
dc.subject | Mitogen-Activated Protein Kinase 10 | |
dc.subject | Mitogen-Activated Protein Kinase 8 | |
dc.subject | Neuroprotective Agents | |
dc.subject | Phosphorylation | |
dc.title | Neuroprotective Effects of the Absence of JNK1 or JNK3 Isoforms on Kainic Acid-Induced Temporal Lobe Epilepsy-Like Symptoms | |
dc.type | Article |