PMID- 15502879
OWN - NLM
STAT- MEDLINE
DCOM- 20051019
LR  - 20191109
IS  - 1076-1551 (Print)
IS  - 1528-3658 (Electronic)
IS  - 1076-1551 (Linking)
VI  - 10
IP  - 1-6
DP  - 2004 Jan-Jun
TI  - Gene expression profile in interleukin-4-stimulated human vascular endothelial 
      cells.
PG  - 19-27
AB  - Interleukin-4 (IL-4)-mediated pro-oxidative and pro-inflammatory vascular 
      environments have been implicated in the pathogenesis of atherosclerosis. The 
      cellular and molecular regulatory mechanisms underlying this process, however, 
      are not fully understood. In the present study, we employed GeneChip microarray 
      analysis to investigate global gene expression patterns in human vascular 
      endothelial cells after treatment with IL-4. Our results showed that mRNA levels 
      of a total of 106 genes were significantly up-regulated and 41 genes 
      significantly down-regulated with more than a 2-fold change. The majority of 
      these genes are critically involved in the regulation of inflammatory responses, 
      apoptosis, signal transduction, transcription factors, and metabolism; functions 
      of the remaining genes are unknown. The changes in gene expression of selected 
      genes related to inflammatory reactions, such as vascular cell adhesion 
      molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), and 
      interleukin-6 (IL-6), were verified by quantitative real-time reverse 
      transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent 
      assay (ELISA) analyses. IL-4 treatment also significantly increased the adherence 
      of inflammatory cells to endothelial cell monolayers in a dose-dependent manner. 
      These results may help determine the molecular mechanisms of action of IL-4 in 
      human vascular endothelium. In addition, a better understanding of IL-4-induced 
      vascular injury at the level of gene expression could lead to the identification 
      of new therapeutic strategies for atherosclerosis.
FAU - Lee, Yong Woo
AU  - Lee YW
AD  - Department of Surgery/Division of Neurosurgery, University of Kentucky College of 
      Medicine, 800 Rose Street, Lexington, Kentucky 40536, USA. ylee2@uky.edu
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Chen, Kuey Chu
AU  - Chen KC
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Mol Med
JT  - Molecular medicine (Cambridge, Mass.)
JID - 9501023
RN  - 0 (Inflammation Mediators)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Apoptosis/genetics
MH  - Cell Line, Tumor
MH  - Endothelial Cells/*drug effects/metabolism
MH  - *Gene Expression Profiling
MH  - Gene Expression Regulation/*drug effects
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Interleukin-4/*pharmacology
MH  - Oligonucleotide Array Sequence Analysis
MH  - RNA, Messenger/metabolism
MH  - Signal Transduction/genetics
MH  - Transcription Factors/genetics
PMC - PMC1431351
EDAT- 2004/10/27 09:00
MHDA- 2005/10/20 09:00
PMCR- 2004/01/01
CRDT- 2004/10/27 09:00
PHST- 2004/10/27 09:00 [pubmed]
PHST- 2005/10/20 09:00 [medline]
PHST- 2004/10/27 09:00 [entrez]
PHST- 2004/01/01 00:00 [pmc-release]
AID - mol10_1p19 [pii]
AID - 10.2119/2004-00024.lee [doi]
PST - ppublish
SO  - Mol Med. 2004 Jan-Jun;10(1-6):19-27. doi: 10.2119/2004-00024.lee.