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Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells

Title
Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells
Authors
Park H.S.Chun J.N.Jung H.Y.Choi C.Bae Y.S.
Ewha Authors
배윤수
SCOPUS Author ID
배윤수scopus
Issue Date
2006
Journal Title
Cardiovascular Research
ISSN
0008-6363JCR Link
Citation
vol. 72, no. 3, pp. 447 - 455
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Objective: We investigated the role of NADPH oxidase 4 (Nox4) on lipopolysaccharide (LPS)-induced proinflammatory responses by human aortic endothelial cells (HAECs). Methods and results: Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (amino acids 739-769) is the responsible domain for interaction with the COOH terminal of Nox4 (amino acids 451-530). Consistently, overexpression of the COOH-terminal region of Nox4 inhibited nuclear factor-κB activation in response to LPS. Downregulation of Nox4 by transfection of siRNA specific to Nox4 in HAECs resulted in a failure to induce reactive oxygen species (ROS) generation and subsequent expression of intercellular adhesion molecule-1 (ICAM-1) and chemokines such as IL-8 and monocyte chemoattractant protein-1 (MCP-1) in response to LPS. Furthermore, transient transfection of endothelial cells with Nox4 siRNA led to a decrease in migration and adhesion of monocytes in response to LPS by 36% and 52%, respectively. Conclusions: Nox4 plays a central role in LPS-induced proinflammatory responses by endothelial cells in an ROS-dependent manner. © 2006 European Society of Cardiology.
DOI
10.1016/j.cardiores.2006.09.012
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자연과학대학 > 생명과학전공 > Journal papers
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