Journal
FEBS LETTERS
Volume 585, Issue 14, Pages 2263-2268Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2011.05.049
Keywords
Mitochondria; Innate immunity; Inflammatory cytokine; Macrophage; Reactive oxygen species; TLR4
Funding
- Ministry of Education, Science, Sports and Culture of Japanese Government [21700698]
- Grants-in-Aid for Scientific Research [21700698] Funding Source: KAKEN
Ask authors/readers for more resources
We investigated the role of mitochondrial reactive oxygen species (ROS) in the response of macrophages to lipopolysaccharide (LPS) using RAW 264.7 cells and their rho(0) cells lacking mitochondria. Mitochondrial density, respiratory activity and related proteins in rho(0) cells were significantly lower than those in RAW cells. LPS rapidly stimulated mitochondrial ROS prior to cytokine secretion, such as TNF-alpha and IL-6, from RAW 264.7 cells by activating the MAPK pathway, while the response was attenuated in rho(0) cells. Exposure of rho(0) cells to H(2)O(2) partially restored the secretion of cytokines induced by LPS. These results suggest that mitochondrial density and/or the respiratory state contribute to intracellular oxidative stress, which is responsible for the stimulation of LPS-induced MAPK signaling to enhance cytokine release from macrophages. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available