{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T05:59:15Z","timestamp":1760853555497},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,5,11]],"date-time":"2012-05-11T00:00:00Z","timestamp":1336694400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuropathology Appl Neurobio"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:p>F. Junyent, L. de Lemos, E. Verdaguer, M. Pall\u00e0s, J. Folch, C. Beas\u2010Z\u00e1rate, A. Camins and C. Auladell (2012) <jats:italic>Neuropathology and Applied Neurobiology<\/jats:italic><jats:bold>38,<\/jats:bold> 311\u2013321<\/jats:p><jats:p><jats:bold>Lack of Jun\u2010N\u2010terminal kinase 3 (JNK3) does not protect against neurodegeneration induced by 3\u2010nitropropionic acid<\/jats:bold><\/jats:p><jats:p><jats:bold>Aims:<\/jats:bold> 3\u2010Nitropropionic acid (3\u2010NP) is a toxin that replicates most of the clinical and pathophysiological symptoms of Huntington's disease, inducing neurodegeneration in the striatum due to the inhibition of mitochondrial succinate dehydrogenase. Different pathways have been implicated in the cell death induced by 3\u2010NP in rodents. One of them is the Jun\u2010N\u2010terminal kinase (JNK) pathway, which may play a role in the neurodegenerative process in different diseases. Moreover, the lack of one isoform of JNK (JNK3) has been associated with neuroprotection in different experimental models of neurodegeneration. Therefore, in the present study the role of JNK3 in the experimental Huntington's model induced by 3\u2010NP administration was evaluated. <jats:bold>Methods:<\/jats:bold> 3\u2010NP was intraperitoneally administered once a day for 3 days to wild\u2010type and <jats:italic>Jnk3<\/jats:italic>\u2010null mice. Coronal brain sections were used to determine cell death and astrogliosis in striatum. Western blots were performed to determine the involvement of different pathways in both wild\u2010type and <jats:italic>Jnk3<\/jats:italic>\u2010null mice. <jats:bold>Results:<\/jats:bold> Although JNK activation was observed following 3\u2010NP administration, the results indicate that the lack of JNK3 does not confer neuroprotection against 3\u2010NP toxicity. Thus, other pathways must be involved in the neurodegeneration induced in this model. One of the possible pathways towards 3\u2010NP\u2010induced apoptosis could involve the calpains, as their activity was increased in wild\u2010type and <jats:italic>Jnk3<\/jats:italic>\u2010null mice. <jats:bold>Conclusion:<\/jats:bold> Although JNK3 is a key protein involved in cell death in different neurodegenerative diseases, the present study demonstrates that the lack of JNK3 does not confer neuroprotection against 3\u2010NP\u2010induced neuronal death.<\/jats:p>","DOI":"10.1111\/j.1365-2990.2011.01214.x","type":"journal-article","created":{"date-parts":[[2011,8,31]],"date-time":"2011-08-31T20:24:46Z","timestamp":1314822286000},"page":"311-321","source":"Crossref","is-referenced-by-count":7,"title":["Lack of Jun\u2010N\u2010terminal kinase 3 (JNK3) does not protect against neurodegeneration induced by 3\u2010nitropropionic 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