PMID- 20349326
OWN - NLM
STAT- MEDLINE
DCOM- 20101130
LR  - 20211020
IS  - 1420-908X (Electronic)
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 59
IP  - 9
DP  - 2010 Sep
TI  - Role of NADPH oxidase in interleukin-4-induced monocyte chemoattractant protein-1 
      expression in vascular endothelium.
PG  - 755-65
LID - 10.1007/s00011-010-0187-3 [doi]
AB  - OBJECTIVE AND DESIGN: The pro-oxidative and pro-inflammatory pathways in vascular 
      endothelium have been implicated in the development of atherosclerosis. In the 
      present study, we investigated effect of interleukin-4 (IL-4) on monocyte 
      chemoattractant protein-1 (MCP-1) expression in vascular endothelium and examined 
      the role of distinct sources of reactive oxygen species (ROS) in this process. 
      METHODS AND RESULTS: Real-time reverse transcriptase-polymerase chain reaction 
      and enzyme-linked immunosorbent assay showed that IL-4 significantly up-regulated 
      mRNA and protein expression of MCP-1 in human aortic endothelial cells (HAEC) and 
      C57BL/6 mice. A significant and dose-dependent inhibition of IL-4-induced MCP-1 
      expression was observed in HAEC pre-treated with antioxidants, such as 
      pyrrolidine dithiocarbamate and epigallocatechin gallate, indicating that 
      IL-4-induced MCP-1 expression is mediated via a ROS-dependent mechanism. 
      Additionally, pharmacological inhibitors of NADPH oxidase (NOX) significantly 
      attenuated IL-4-induced MCP-1 expression in HAEC. Furthermore, the disruption of 
      the NOX gene dramatically reduced IL-4-induced MCP-1 expression in NOX knockout 
      mice (B6.129S6-Cybb(tm1Din)/J). In contrast, overexpression of MCP-1 in 
      IL-4-stimulated HAEC was not affected by inhibiting other ROS generating 
      pathways, such as xanthine oxidase and the mitochondrial electron transport 
      chain. CONCLUSIONS: These results demonstrate that IL-4 up-regulates MCP-1 
      expression in vascular endothelium through NOX-mediated ROS generation.
FAU - Lee, Yong Woo
AU  - Lee YW
AD  - Department of Biomedical Sciences and Pathobiology, School of Biomedical 
      Engineering and Sciences, Virginia Polytechnic Institute and State University 
      (Virginia Tech), Blacksburg, VA 24061, USA. ywlee@vt.edu
FAU - Lee, Won Hee
AU  - Lee WH
FAU - Kim, Paul H
AU  - Kim PH
LA  - eng
GR  - R15 HL085229/HL/NHLBI NIH HHS/United States
GR  - R15 HL085229-01A1/HL/NHLBI NIH HHS/United States
GR  - HL085229/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20100328
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 207137-56-2 (Interleukin-4)
RN  - EC 1.6.3.- (NADPH Oxidases)
SB  - IM
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Aorta/drug effects/enzymology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - Endothelium, Vascular/*drug effects/enzymology/*metabolism
MH  - Humans
MH  - Interleukin-4/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NADPH Oxidases/analysis/antagonists & inhibitors/*metabolism
MH  - Up-Regulation/drug effects
PMC - PMC2916038
MID - NIHMS194801
EDAT- 2010/03/30 06:00
MHDA- 2010/12/14 06:00
PMCR- 2011/09/01
CRDT- 2010/03/30 06:00
PHST- 2009/09/14 00:00 [received]
PHST- 2010/03/05 00:00 [accepted]
PHST- 2010/01/12 00:00 [revised]
PHST- 2010/03/30 06:00 [entrez]
PHST- 2010/03/30 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
PHST- 2011/09/01 00:00 [pmc-release]
AID - 10.1007/s00011-010-0187-3 [doi]
PST - ppublish
SO  - Inflamm Res. 2010 Sep;59(9):755-65. doi: 10.1007/s00011-010-0187-3. Epub 2010 Mar 
      28.