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Upregulation of Daxx mediates apoptosis in response to oxidative stress

✍ Scribed by Kyung Soon Kim; Hyun-Ah Hwang; Suhn-Kee Chae; Hyunjung Ha; Ki-Sun Kwon

Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
250 KB
Volume
96
Category
Article
ISSN
0730-2312

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✦ Synopsis

Abstract

Oxidative stress induces apoptosis in a variety of cell types by as yet unclear signaling mechanisms. The Daxx protein is reportedly involved in apoptosis through its interactions with Fas, transforming growth factor‐β receptor, and promyelocytic leukemia protein (PML). Here, we explored the possible roles of Daxx in oxidative stress‐induced apoptosis. We found that both the mRNA and protein levels of Daxx markedly increased when cells underwent apoptosis after H~2~O~2~ treatment. Pretreatment with the cell‐permeable antioxidant, N‐acetyl cysteine, prevented cells from H~2~O~2~‐induced Daxx upregulation and subsequent apoptosis, indicating that the endogenous oxidant regulated Daxx expression. Furthermore, suppression of endogenous Daxx expression by antisense oligonucleotide technology inhibited oxidative stress‐induced apoptosis in HeLa cells. Taken together, these results suggest that Daxx acts as an intermediary messenger of pro‐apoptotic signals triggered by oxidative stress. © 2005 Wiley‐Liss, Inc.

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