Anamorsin attenuates cupric chloride-induced dopaminergic neuronal cell death.

Neurodegenerative diseases are associated with elevated levels of metal elements, which are well-known inducers of reactive oxygen species in cells. Because dopaminergic neurons in the substantia nigra are vulnerable to dysregulation of metals and the resulting accumulation of could be a cause of dopaminergic neurodegeneration. In this study, we showed that overexpression of anamorsin protected MN9D dopaminergic neuronal cells from cupric chloride-induced death. This cytoprotection was achieved by specifically decreasing duanyu1670 levels. As determined by mini two-dimensional electrophoretic assay, an acidic shift of anamorsin occurred during drug-induced death, which seemed to be mediated by oxidative modification of three of its CXXC motifs. Consequently, drug-induced dissociation of ASK1 from Trx1 and subsequent phosphorylation of JNK and p38 MAPK were inhibited in MN9D cells overexpressing anamorsin. Taken together, our results indicate that anamorsin exerts a neuroprotective effect by reducing intracellular duanyu1670 levels and subsequently attenuating activated stress-activated MAP kinases pathways.

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