Down-regulation of endothelial cell estrogen receptor expression by the inflammation promoter LPS

Anders E Holm, Kristina E. Andersson, Ina Nordström, Per Hellstrand, Bengt Olof Nilsson

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Endothelial cells express both estrogen receptor (ER) α and β. The objective of this study was to investigate if and how mediators of inflammation regulate endothelial cell ERα and ERβ expression. ERα and ERβ transcript and protein expression were determined by real-time quantitative PCR and Western blotting, respectively, in endothelial cell line bEnd.3 cells stimulated with the inflammation promoter lipopolysaccharide (E. coli LPS). Stimulation with LPS (500 ng/ml and 10 μg/ml) for 4 days reduced both ERα and ERβ mRNA levels. The glucocorticoid dexamethasone (1 μM) had no effect on LPS-induced attenuation of ERα and β transcript expression. Full-length 66-67 kDa ERα protein was unaffected by 4 days stimulation with LPS, while the 46-kDa ERα isoform was reduced by about 20%. ERβ protein was reduced by about 40% by LPS at 4 days. Treatment with 17β-estradiol (E2, 100 nM) for 4 days increased ERβ mRNA by about 8 times but had no effect on ERα mRNA level. The E2-induced increase in ERβ transcript was not associated with increased ERβ protein. E2 increased ERβ mRNA expression also in the presence of LPS, suggesting that inflammation-induced impairment of ERβ signalling is rescued by estrogen.

Original languageEnglish (US)
Pages (from-to)8-13
Number of pages6
JournalMolecular and Cellular Endocrinology
Issue number1-2
StatePublished - May 5 2010


  • 17β-Estradiol
  • Endothelial cells
  • Estrogen receptor α and β
  • Inflammation
  • LPS


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