Role of NADPH oxidase-2 in lipopolysaccharide-induced matrix metalloproteinase expression and cell migration

Title
Role of NADPH oxidase-2 in lipopolysaccharide-induced matrix metalloproteinase expression and cell migration
Author(s)
백석환김소연이진구조우성[조우성]조경현사공준김재룡
Keywords
NECROSIS-FACTOR-ALPHA; OXIDATIVE STRESS; EPITHELIAL-CELLS; SUPEROXIDE-PRODUCTION; HUMAN ATHEROSCLEROSIS; ENDOTHELIAL-CELLS; TYROSINE KINASE; NAD(P)H OXIDASE; SMOOTH-MUSCLE; ACTIVATION
Issue Date
201002
Publisher
NATURE PUBLISHING GROUP
Citation
IMMUNOLOGY AND CELL BIOLOGY, v.88, no.2, pp.197 - 204
Abstract
This study examined the hypothesis that the control of NADPH oxidase-2 (Nox2)-mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Lipopolysaccharide (LPS) stimulation of Raw264.7 cells and mice peritoneal macrophages increased the expression of MMP-9, 10, 12 and 13 mRNA, and also increased Raw264.7 cell migration. Treatment with an antioxidant (N-acetyl cysteine) or Nox inhibitors strongly inhibited the expression of MMPs by LPS and inhibited cell migration. LPS caused ROS production in macrophages and increased the mRNA expression of Nox isoforms Nox1 and Nox2 by 20-fold and two-fold, respectively. While Nox1 small interfering RNA (siRNA) did not inhibit LPS-mediated expression of MMPs, Nox2 siRNA inhibited the expressions of MMP-9, 10 and 12. Neither Nox1 nor Nox2 siRNA influenced the LPS-mediated expression of MMP-13. In addition, NAC or apocynin attenuated LPS-induced ROS production and MMP-9 expression. MMP-9 expression and cell migration were controlled by ERK1/2-ROS signaling. Collectively, these results suggest that LPS stimulates ROS production via ERK and induce various types of MMPs expression and cell migration. Immunology and Cell Biology (2010) 88, 197-204; doi:10.1038/icb.2009.87; published online 24 November 2009
URI
http://hdl.handle.net/YU.REPOSITORY/22939http://dx.doi.org/10.1038/icb.2009.87
ISSN
0818-9641
Appears in Collections:
의과대학 > 생화학.분자생물학교실 > Articles
생명공학부 > 생명공학부 > Articles
의과대학 > 예방의학교실 > Articles
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