Oxidative stress induces PKR-dependent apoptosis via IFN-gamma activation signaling in Jurkat T cells
- Authors
- Pyo, Chul-Woong; Lee, Shin-Hee; Choi, Sang-Yun
- Issue Date
- 19-12월-2008
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- ROS; Interferon; PKR; Apoptosis
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.377, no.3, pp.1001 - 1006
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 377
- Number
- 3
- Start Page
- 1001
- End Page
- 1006
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/122205
- DOI
- 10.1016/j.bbrc.2008.10.103
- ISSN
- 0006-291X
- Abstract
- The dsRNA-dependent protein kinase, PKR, is a central component in antiviral defense. The biological importance of PKR is further remarked by its critical role in apoptosis induced by a variety of stresses. Here, we analyzed the implication of oxidative stress in the induction of PKR-dependent apoptosis in Jurkat cells. Our results revealed that reactive oxygen species (ROS) induced endogenous pkr gene expression at the transcriptional level by activating the interferon (IFN)-gamma gene. However, IFN-gamma siRNA expression abrogated the H2O2-mediated pkr induction. The radical scavenger N-acetyl-L-cysteine profoundly inhibited pkr induction via the reduction of IFN-gamma expression. The treatment of cells with the specific JAK-STAT inhibitor, AG490, reduced the PKR expression, and Suppressed PKR-dependent cell death. Finally, siRNA-mediated depletion of IFN-gamma or pkr efficiently downregulated H2O2-mediated apoptotic cell death. These results indicated that oxidative stress induces PKR expression essentially via the IFN-gamma activation signal, and causes apoptosis in Jurkat T cells. (C) 2008 Elsevier Inc. All rights reserved.
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