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Characterization of catechol-thioether-induced apoptosis in human SH-SY5Y neuroblastoma cells

✍ Scribed by Luciana Mosca; Italo Tempera; Eugenio Lendaro; Laura Di Francesco; Maria d'Erme

Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
231 KB
Volume
86
Category
Article
ISSN
0360-4012

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✦ Synopsis

Abstract

Recent work has highlighted the involvement of a dopamine derivative, 5‐S‐cysteinyl‐dopamine (CysDA), in neurodegeneration and apoptotic cell death. In this paper we study in further detail the apoptotic process activated by this catechol‐thioether derivative of dopamine in SH‐SY5Y neuroblastoma cells. CysDA activates a cascade of events by an initial perturbation of Calcium homeostasis in the cell. Cell treatment with the catechol‐thioether induces an immediate rise in intracellular Ca^2+^ concentration, as demonstrated by a shift in the indo‐1 dye emission spectrum, and a sustained high calcium concentration at long times of incubation. Fluorescence microscopy data show that the treatment of cells induces mitochondrial transmembrane potential depolarization, a clear evidence of the onset of apoptotic process. Programmed cell death activation is also demonstrated by cytochrome c release from the mitochondria, by an increased activity of both caspase‐8 and ‐9 and by the poly(ADP‐ribose)polymerase (PARP‐1) cleavage, yielding the typical 86 kDa fragment due to caspase‐3 activity. Overall, our data support the hypothesis that CysDA may induce apoptotic death in neuronal cells, via an initial perturbation of calcium homeostasis in the cytosol. © 2007 Wiley‐Liss, Inc.

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