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자연과학대학
생명과학전공
Journal papers
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Flagellin-induced NADPH oxidase 4 activation is involved in atherosclerosis
Title
Flagellin-induced NADPH oxidase 4 activation is involved in atherosclerosis
Authors
Kim J.
;
Seo M.
;
Kim S.K.
;
Bae Y.S.
Ewha Authors
배윤수
SCOPUS Author ID
배윤수
Issue Date
2016
Journal Title
Scientific Reports
ISSN
2045-2322
Citation
Scientific Reports vol. 6
Publisher
Nature Publishing Group
Indexed
SCIE; SCOPUS
Document Type
Article
Abstract
It is widely accepted that bacterial infection-mediated inflammation facilitates development of atherosclerosis by activating toll-like receptor (TLR) signaling system. We reasoned that NADPH oxidases (Nox), required for TLR-mediated inflammatory response, are involved in atherogenesis. Here, we show that the activation of Nox4 through TLR5 regulates the inflammation of the endothelium and in atherogenesis. Flagellin-induced interaction between the COOH region of Nox4 and the TIR domain of TLR5 led to H2O2 generation, which in turn promoted the secretion of pro-inflammatory cytokines including IL-8, as well as the expression of ICAM-1 in human aortic endothelial cells (HAECs). Knockdown of the Nox4 in HAECs resulted in attenuated expressions of IL-8 and ICAM-1 leading to a reduction in the adhesion and trans-endothelial migration of monocytes. Challenge of recombinant FliC (rFliC) to the ApoE KO mice with high-fat diet (HFD) resulted in significantly increased atherosclerotic plaque sizes compared to the saline-injected mice. However, an injection of rFliC into the Nox4ApoE DKO mice with HFDs failed to generate atherosclerotic plaque, suggesting that Nox4 deficiency resulted in significant protections against rFliC-mediated atherogenesis. We conclude that TLR5-dependent Nox4 activation and subsequent H2O2 generation play critical roles for the development of atherosclerosis. © 2016, Nature Publishing Group. All rights reserved.
DOI
10.1038/srep25437
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