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

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

Research output: Contribution to journalArticlepeer-review

44 Citations (SciVal)

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.
Original languageEnglish
Pages (from-to)349-353
JournalInflammation Research
Volume55
Issue number8
DOIs
Publication statusPublished - 2006

Subject classification (UKÄ)

  • Rheumatology and Autoimmunity

Keywords

  • gene expression-LPS
  • inflammation
  • arteries
  • estrogen

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