Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 배윤수 | * |
dc.date.accessioned | 2016-08-29T12:08:50Z | - |
dc.date.available | 2016-08-29T12:08:50Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 2045-2322 | * |
dc.identifier.other | OAK-18674 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/231572 | - |
dc.description.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. | * |
dc.language | English | * |
dc.publisher | Nature Publishing Group | * |
dc.title | Flagellin-induced NADPH oxidase 4 activation is involved in atherosclerosis | * |
dc.type | Article | * |
dc.relation.volume | 6 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Scientific Reports | * |
dc.identifier.doi | 10.1038/srep25437 | * |
dc.identifier.wosid | WOS:000375539600003 | * |
dc.identifier.scopusid | 2-s2.0-84966415502 | * |
dc.author.google | Kim J. | * |
dc.author.google | Seo M. | * |
dc.author.google | Kim S.K. | * |
dc.author.google | Bae Y.S. | * |
dc.contributor.scopusid | 배윤수(15031067200) | * |
dc.date.modifydate | 20240415133331 | * |