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Interaction of NADPH oxidase 1 with Toll-like receptor 2 induces migration of smooth muscle cells

Title
Interaction of NADPH oxidase 1 with Toll-like receptor 2 induces migration of smooth muscle cells
Authors
Lee, Jee HyunJoo, Jung HeeKim, JinohLim, Hee JungKim, SunahCurtiss, LindaSeong, Je KyungCui, WenhaoYabe-Nishimura, ChihiroBae, Yun Soo
Ewha Authors
배윤수주정희
SCOPUS Author ID
배윤수scopus; 주정희scopusscopus
Issue Date
2013
Journal Title
CARDIOVASCULAR RESEARCH
ISSN
0008-6363JCR Link
Citation
vol. 99, no. 3, pp. 483 - 493
Keywords
Toll-like receptor 2NADPH oxidasereactive oxygen speciesmouse aortic smooth muscle cellsmacrophage inflammatory protein 2
Publisher
OXFORD UNIV PRESS
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
NADPH oxidase (Nox) isozymes that generate intracellular reactive oxygen species (ROS) and Toll-like receptor 2 (TLR2), an inflammatory mediator, are both involved in the development of atherosclerotic lesions. To identify the molecular connection between TLR2 and Nox isozymes in vascular remodelling, we analysed generation of ROS and pro-inflammatory cytokines in aortic smooth muscle cells from Nox1-deficient mice in response to the synthetic triacylated lipoprotein Pam3CSK, a TLR2 agonist. We showed that TLR2 signalling stimulates progression of the pro-inflammatory phenotype in mouse aortic smooth muscle cells (MASMCs) through activation of Nox1. We demonstrated the interaction of TLR2 with Nox1 using yeast two-hybrid and co-immunoprecipitation assays. MASMCs from Nox1-deficient mice failed to generate of ROS in response to Pam3CSK4, indicating that Nox1 is essential for TLR2-dependent production of ROS. We also found that Pam3CSK4 stimulated migration of MASMCs from wild-type mice in a Transwell system, but MASMCs from Nox1-deficient mice failed to show this response. Wild-type MASMCs produced matrix metalloprotease 2 in response to Pam3CSK4, whereas Nox1-deficient MASMCs failed to generate this protease. Moreover, stimulation of MASMCs with Pam3CSK4 resulted in increased expression of the pro-inflammatory cytokine macrophage inflammatory protein 2 in a Nox1-dependent manner, leading to enhanced monocyte-endothelial cell adhesion and trans-endothelial migration of U937 cells. These data suggest that Nox1 plays an important role in TLR2-mediated intracellular H2O2 generation, activation of matrix metalloprotease 2, and secretion of pro-inflammatory cytokines, which in turn stimulate MASMC migration and vascular remodelling.
DOI
10.1093/cvr/cvt107
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자연과학대학 > 생명과학전공 > Journal papers
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