PMID: 12764057May 24, 2003Paper

TNF-induced death of adult human oligodendrocytes is mediated by c-jun NH2-terminal kinase-3

Brain : a Journal of Neurology
Anna JurewiczKrzysztof Selmaj

Abstract

Tumour necrosis factor (TNF) induces death of oligodendrocytes, the putative cell target in multiple sclerosis. We defined that the intracellular transduction pathway involved in TNF-induced death of human adult oligodendrocytes (hOLs) is dependent on c-jun NH(2)-terminal kinase (JNK) activation, but not the other mitogen-activated protein kinase (MAPK), p38. JNK activation, measured by c-jun phosphorylation and induction of the phosphorylated form of JNK, was enhanced, prolonged and correlated with cell death in hOLs exposed to TNF. Comparative autoradiographic analysis revealed that JNK-3, but not JNK-1 or JNK-2, is responsible for prolonged JNK activation in TNF exposed hOLs. Expression of a dominant-negative mutant of JNK upstream kinase, MKK4/SEK1, inhibited apoptosis induced by TNF, whereas expression of a constitutive active mutant of MEKK1, an upstream kinase to JNK, accelerates TNF-induced apoptosis. JNK activation occurred prior to changes of mitochondrial membrane potential in hOLs exposed to TNF. These results demonstrate that TNF-induced death in adult hOLs depends on prolonged JNK-3 activation, and that this apoptosis requires the mitochondrial dysfunction that occurs after JNK activation. This is the first eviden...Continue Reading

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Citations

Nov 13, 2007·Journal of Molecular Neuroscience : MN·Jeffery D HainesGuillermina Almazan
Apr 28, 2012·Molecular Neurobiology·Margarida Castro-CaldasMaria João Gama
Apr 11, 2009·Brain : a Journal of Neurology·Alessia MelaniFelicita Pedata
Feb 17, 2010·Brain : a Journal of Neurology·Sara VetoZsolt Illes
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