PMID- 17064675
OWN - NLM
STAT- MEDLINE
DCOM- 20070709
LR  - 20220225
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 72
IP  - 3
DP  - 2006 Dec 1
TI  - Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses 
      by human aortic endothelial cells.
PG  - 447-55
AB  - 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-kappaB 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.
FAU - Park, Hye Sun
AU  - Park HS
AD  - Division of Molecular Life Sciences, Center for Cell Signaling Research, Ewha 
      Womans University, 11-1 Daehyun-Dong, Seodaemoon-Gu, Seoul 120-750, Republic of 
      Korea.
FAU - Chun, Jung Nyeo
AU  - Chun JN
FAU - Jung, Hye Young
AU  - Jung HY
FAU - Choi, Chulhee
AU  - Choi C
FAU - Bae, Yun Soo
AU  - Bae YS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060923
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Small Interfering)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.6.3.- (NADPH Oxidase 4)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.- (NOX4 protein, human)
SB  - IM
MH  - Aorta
MH  - Bacterial Infections/enzymology/*immunology
MH  - Cell Adhesion/drug effects
MH  - Cell Movement/drug effects
MH  - Cell Nucleus/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/analysis
MH  - Endothelial Cells/enzymology/*immunology
MH  - Humans
MH  - Hydrogen Peroxide/analysis
MH  - Intercellular Adhesion Molecule-1/analysis
MH  - Interleukin-8/analysis
MH  - Lipopolysaccharides/pharmacology
MH  - Monocytes/drug effects
MH  - NADPH Oxidase 4
MH  - NADPH Oxidases/genetics/*physiology
MH  - NF-kappa B/metabolism
MH  - Protein Binding
MH  - RNA Interference
MH  - RNA, Small Interfering/pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transfection/methods
MH  - Two-Hybrid System Techniques
EDAT- 2006/10/27 09:00
MHDA- 2007/07/10 09:00
CRDT- 2006/10/27 09:00
PHST- 2006/05/03 00:00 [received]
PHST- 2006/07/21 00:00 [revised]
PHST- 2006/09/18 00:00 [accepted]
PHST- 2006/10/27 09:00 [pubmed]
PHST- 2007/07/10 09:00 [medline]
PHST- 2006/10/27 09:00 [entrez]
AID - S0008-6363(06)00411-1 [pii]
AID - 10.1016/j.cardiores.2006.09.012 [doi]
PST - ppublish
SO  - Cardiovasc Res. 2006 Dec 1;72(3):447-55. doi: 10.1016/j.cardiores.2006.09.012. 
      Epub 2006 Sep 23.