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Estrogen attenuates vascular expression of inflammation associated genes and adhesion of monocytes to endothelial cells

Gao, H. ; Liang, Min LU ; Bergdahl, Andreas LU ; Hamren, A ; Lindholm, Marie LU ; Dahlman-Wright, K. and Nilsson, Bengt-Olof LU orcid (2006) In Inflammation Research 55(8). p.349-353
Abstract
Objective: Investigate effects of estrogen at gene expression and functional levels in vascular wall cells treated with bacterial lipopolysaccharide (LPS). Materials and methods: Aortic segments from ovariectomized mice were treated with LPS for 24 h in the absence or presence of 17 beta-estradiol (E-2). Gene activity was determined by Affymetrix microarray analysis and real-time RTPCR. Adhesion of [H-3]-thymidine labelled human THP-1 monocytes to mouse bEnd.3 endothelial cells was determined by measuring radioactivity of DNA from co-culture homogenates. Results: Analysis of global gene expression profiles revealed that 10 nM E-2 attenuates LPS-induced (10 ng/ml) expression of genes coding for well-known acute-phase proteins, such as... (More)
Objective: Investigate effects of estrogen at gene expression and functional levels in vascular wall cells treated with bacterial lipopolysaccharide (LPS). Materials and methods: Aortic segments from ovariectomized mice were treated with LPS for 24 h in the absence or presence of 17 beta-estradiol (E-2). Gene activity was determined by Affymetrix microarray analysis and real-time RTPCR. Adhesion of [H-3]-thymidine labelled human THP-1 monocytes to mouse bEnd.3 endothelial cells was determined by measuring radioactivity of DNA from co-culture homogenates. Results: Analysis of global gene expression profiles revealed that 10 nM E-2 attenuates LPS-induced (10 ng/ml) expression of genes coding for well-known acute-phase proteins, such as alpha-trypsin inhibitor heavy chain 4, serum amyloid A3 and lipocalin 2. The E-2-induced down-regulation of these three genes observed by microarray was confirmed by realtime RT-PCR. Treatment with 500ng/ml LPS increased adhesion of monocytes to endothelial cells more than two fold. Importantly, LPS-induced monocyte adhesion was fully prevented by 50nM E-2. Conclusion: Estrogen reduces expression of acute-phase protein genes and inhibits LPS-induced moncocyte adhesion to endothelial cells, suggesting that estrogen might have a vasculoprotective effect via this mechanism. (Less)
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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
gene expression-LPS, inflammation, arteries, estrogen
in
Inflammation Research
volume
55
issue
8
pages
349 - 353
publisher
Birkhäuser Verlag
external identifiers
  • wos:000239928400005
  • scopus:33748851388
ISSN
1420-908X
DOI
10.1007/s00011-006-5194-z
language
English
LU publication?
yes
id
9e4f0aba-f7db-4f13-8dcd-b3ac682ac7a9 (old id 397425)
date added to LUP
2016-04-01 12:12:16
date last changed
2022-03-05 20:22:14
@article{9e4f0aba-f7db-4f13-8dcd-b3ac682ac7a9,
  abstract     = {{Objective: Investigate effects of estrogen at gene expression and functional levels in vascular wall cells treated with bacterial lipopolysaccharide (LPS). Materials and methods: Aortic segments from ovariectomized mice were treated with LPS for 24 h in the absence or presence of 17 beta-estradiol (E-2). Gene activity was determined by Affymetrix microarray analysis and real-time RTPCR. Adhesion of [H-3]-thymidine labelled human THP-1 monocytes to mouse bEnd.3 endothelial cells was determined by measuring radioactivity of DNA from co-culture homogenates. Results: Analysis of global gene expression profiles revealed that 10 nM E-2 attenuates LPS-induced (10 ng/ml) expression of genes coding for well-known acute-phase proteins, such as alpha-trypsin inhibitor heavy chain 4, serum amyloid A3 and lipocalin 2. The E-2-induced down-regulation of these three genes observed by microarray was confirmed by realtime RT-PCR. Treatment with 500ng/ml LPS increased adhesion of monocytes to endothelial cells more than two fold. Importantly, LPS-induced monocyte adhesion was fully prevented by 50nM E-2. Conclusion: Estrogen reduces expression of acute-phase protein genes and inhibits LPS-induced moncocyte adhesion to endothelial cells, suggesting that estrogen might have a vasculoprotective effect via this mechanism.}},
  author       = {{Gao, H. and Liang, Min and Bergdahl, Andreas and Hamren, A and Lindholm, Marie and Dahlman-Wright, K. and Nilsson, Bengt-Olof}},
  issn         = {{1420-908X}},
  keywords     = {{gene expression-LPS; inflammation; arteries; estrogen}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{349--353}},
  publisher    = {{Birkhäuser Verlag}},
  series       = {{Inflammation Research}},
  title        = {{Estrogen attenuates vascular expression of inflammation associated genes and adhesion of monocytes to endothelial cells}},
  url          = {{http://dx.doi.org/10.1007/s00011-006-5194-z}},
  doi          = {{10.1007/s00011-006-5194-z}},
  volume       = {{55}},
  year         = {{2006}},
}