QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, D. K. Articles by Um, H.-D. Search for Related Content PubMed PubMed Citation Articles by Kim, D. K. Articles by Um, H.-D. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB HYDROGEN PEROXIDE Social Bookmarking                         What's this?

Adaptive concentrations of hydrogen peroxide suppress cell death by blocking the activation of SAPK/JNK pathway

¹ Laboratory of Cell Biology, Yonsei Medical Research Center, Yonsei University College of Medicine, CPO Box 8044, Seoul 120-752, Korea
² Department of Laboratory Animal Science, Yonsei Medical Research Center, Yonsei University College of Medicine, CPO Box 8044, Seoul 120-752, Korea
³ Brain Korea 21 Center for Medical Sciences, Yonsei University College of Medicine, CPO Box 8044, Seoul 120-752, Korea

*Author for correspondence (e-mail: hdum{at}yumc.yonsei.ac.kr)

Accepted August 13, 2001

Low levels of H₂O₂ can induce cellular resistance to subsequent higher levels of H₂O₂. By using human U937 leukemia cells, it was previously shown that such an adaptive response can be induced without increasing the cellular capacity to degrade H₂O₂, thus conferring on the cells a cross-resistance to other stimuli such as serum withdrawal and C₂-ceramide. In this study, it was found that stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) acts as a common mediator of the cell death induced by high H₂O₂ concentrations, serum withdrawal and C₂-ceramide. Although SAPK/JNK activation by H₂O₂ was mediated by two upstream mitogen-activated protein kinase (MAPK) kinases MKK4 and MKK7, only MKK7 played such a role in serum withdrawal and C₂-ceramide. Interestingly, all these lethal stimuli failed to activate SAPK/JNK and its upstream kinases in the cells that were pretreated with low adaptive concentrations of H₂O₂. By contrast, the phosphorylation levels of extracellular signal-regulated kinase and p38 MAPK were not significantly influenced by this H₂O₂ pretreatment. Inducing the SAPK/JNK-suppressing effect of H₂O₂ required a time lag, which correlated with the time lag required for the induction of the adaptive response. Overall, the results suggest that H₂O₂ adaptation confers on cells a resistance to multiple stimuli by specifically blocking their ability to activate the SAPK/JNK pathways.

Key words: Adaptation, SAPK/JNK, Hydrogen peroxide, Oxidative stress, Cell death

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				I. H. Bae, M.-J. Park, S. H. Yoon, S. W. Kang, S.-S. Lee, K.-M. Choi, and H.-D. Um Bcl-w Promotes Gastric Cancer Cell Invasion by Inducing Matrix Metalloproteinase-2 Expression via Phosphoinositide 3-Kinase, Akt, and Sp1. Cancer Res., May 15, 2006; 66(10): 4991 - 4995. [Abstract] [Full Text] [PDF]

				J. Wang, H. He, L. Yu, H. H.-x. Xia, M. C. M. Lin, Q. Gu, M. Li, B. Zou, X. An, B. Jiang, et al. HSF1 Down-regulates XAF1 through Transcriptional Regulation J. Biol. Chem., February 3, 2006; 281(5): 2451 - 2459. [Abstract] [Full Text] [PDF]

				H. W. Lee, S.-S. Lee, S. J. Lee, and H.-D. Um Bcl-w Is Expressed in a Majority of Infiltrative Gastric Adenocarcinomas and Suppresses the Cancer Cell Death by Blocking Stress-activated Protein Kinase/c-Jun NH2-terminal Kinase Activation Cancer Res., March 1, 2003; 63(5): 1093 - 1100. [Abstract] [Full Text] [PDF]