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

På svenska

Author

  • H. Gao
  • Min Liang
  • Andreas Bergdahl
  • A Hamren
  • Marie Lindholm
  • K. Dahlman-Wright
  • Bengt-Olof Nilsson

Summary, in English

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.

Publishing year

2006

Language

English

Pages

349-353

Publication/Series

Inflammation Research

Volume

55

Issue

8

Document type

Journal article

Publisher

Birkhäuser Verlag

Topic

  • Rheumatology and Autoimmunity

Keywords

  • gene expression-LPS
  • inflammation
  • arteries
  • estrogen

Status

Published

Research group

  • Vascular Physiology
  • Cardiovascular Research - Immunity and Atherosclerosis

ISBN/ISSN/Other

  • ISSN: 1420-908X