NDLI: Molecular mechanisms of survival and apoptosis in RAW 264.7 macrophages under oxidative stress

Content Provider	Springer Nature Link
Author	Zhang, Y. Fong, C. C. Wong, M. S. Tzang, C. H. Lai, W. P. Fong, W. F. Sui, S. F. Yang, M.
Copyright Year	2005
Abstract	Organisms living in an aerobic environment are continuously exposed to reactive oxygen species (ROS). Apoptosis of cells can be induced by ROS and cells also develop negative feedback mechanisms to limit ROS induced cell death. In this study, RAW264.7 murine macrophage cells were treated with H2O2 and cDNA microarray technique was used to produce gene expression profiles. We found that H2O2 treatment caused up-regulation of stress, survival and apoptosis related genes, and down-regulation of growth and cell cycle promoting genes. Numerous genes of metabolism pathways showed special expression patterns under oxidative stress: glycolysis and lipid synthesis related genes were down-regulated whereas the genes of lipid catabolism and protein synthesis were up-regulated. We also identified several signaling molecules as ROS-responsive, including p53, Akt, NF-κ B, ERK, JNK, p38, PKC and INF-γ . They played important roles in the process of apoptosis or cell survival. Finally, an interactive pathway involved in cellular response to oxidative stress was proposed to provide some insight into the molecular events of apoptosis induced by ROS and the feedback mechanisms involved in cell survival.
Starting Page	545
Ending Page	556
Page Count	12
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	10
Issue Number	3
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2005-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	apoptosis and survival cDNA microarray hydrogen peroxide RAW 264.7 macrophages reactive oxygen species Cancer Research Virology Oncology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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