| Title |
Neuroprotective Effects of the Absence of JNK1 or JNK3 Isoforms on Kainic Acid-Induced Temporal Lobe Epilepsy-Like Symptoms
|
|---|---|
| Published in |
Molecular Neurobiology, June 2017
|
| DOI | 10.1007/s12035-017-0669-1 |
| Pubmed ID | |
| Authors |
Luisa de Lemos, Felix Junyent, Antoni Camins, Rubén Darío Castro-Torres, Jaume Folch, Jordi Olloquequi, Carlos Beas-Zarate, Ester Verdaguer, Carme Auladell |
| Abstract |
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. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 58 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 58 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 17 | 29% |
| Researcher | 7 | 12% |
| Student > Master | 6 | 10% |
| Student > Ph. D. Student | 5 | 9% |
| Student > Doctoral Student | 3 | 5% |
| Other | 8 | 14% |
| Unknown | 12 | 21% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 13 | 22% |
| Neuroscience | 8 | 14% |
| Agricultural and Biological Sciences | 7 | 12% |
| Pharmacology, Toxicology and Pharmaceutical Science | 5 | 9% |
| Medicine and Dentistry | 5 | 9% |
| Other | 6 | 10% |
| Unknown | 14 | 24% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 01 July 2017.
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#18,558,284
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Outputs from Molecular Neurobiology
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Outputs of similar age from Molecular Neurobiology
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