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

Holm, Anders LU ; Andersson, Kristina E LU ; Nordström, Ina LU ; Hellstrand, Per LU and Nilsson, Bengt-Olof LU orcid (2010) In Molecular and Cellular Endocrinology 319. p.8-13
Abstract
Endothelial cells express both estrogen receptor (ER) alpha and beta. The objective of this study was to investigate if and how mediators of inflammation regulate endothelial cell ERalpha and ERbeta expression. ERalpha and ERbeta 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 (500ng/ml and 10mug/ml) for 4 days reduced both ERalpha and ERbeta mRNA levels. The glucocorticoid dexamethasone (1muM) had no effect on LPS-induced attenuation of ERalpha and beta transcript expression. Full-length 66-67kDa ERalpha protein was unaffected by 4 days... (More)
Endothelial cells express both estrogen receptor (ER) alpha and beta. The objective of this study was to investigate if and how mediators of inflammation regulate endothelial cell ERalpha and ERbeta expression. ERalpha and ERbeta 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 (500ng/ml and 10mug/ml) for 4 days reduced both ERalpha and ERbeta mRNA levels. The glucocorticoid dexamethasone (1muM) had no effect on LPS-induced attenuation of ERalpha and beta transcript expression. Full-length 66-67kDa ERalpha protein was unaffected by 4 days stimulation with LPS, while the 46-kDa ERalpha isoform was reduced by about 20%. ERbeta protein was reduced by about 40% by LPS at 4 days. Treatment with 17beta-estradiol (E(2), 100nM) for 4 days increased ERbeta mRNA by about 8 times but had no effect on ERalpha mRNA level. The E(2)-induced increase in ERbeta transcript was not associated with increased ERbeta protein. E(2) increased ERbeta mRNA expression also in the presence of LPS, suggesting that inflammation-induced impairment of ERbeta signalling is rescued by estrogen. (Less)
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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Molecular and Cellular Endocrinology
volume
319
pages
8 - 13
publisher
Elsevier
external identifiers
  • wos:000276438000002
  • pmid:20079402
  • scopus:77249095014
  • pmid:20079402
ISSN
1872-8057
DOI
10.1016/j.mce.2010.01.002
language
English
LU publication?
yes
id
3a369c38-5359-4df6-ba3a-545c2c60dfae (old id 1541024)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20079402?dopt=Abstract
date added to LUP
2016-04-04 07:20:30
date last changed
2022-01-29 02:05:47
@article{3a369c38-5359-4df6-ba3a-545c2c60dfae,
  abstract     = {{Endothelial cells express both estrogen receptor (ER) alpha and beta. The objective of this study was to investigate if and how mediators of inflammation regulate endothelial cell ERalpha and ERbeta expression. ERalpha and ERbeta 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 (500ng/ml and 10mug/ml) for 4 days reduced both ERalpha and ERbeta mRNA levels. The glucocorticoid dexamethasone (1muM) had no effect on LPS-induced attenuation of ERalpha and beta transcript expression. Full-length 66-67kDa ERalpha protein was unaffected by 4 days stimulation with LPS, while the 46-kDa ERalpha isoform was reduced by about 20%. ERbeta protein was reduced by about 40% by LPS at 4 days. Treatment with 17beta-estradiol (E(2), 100nM) for 4 days increased ERbeta mRNA by about 8 times but had no effect on ERalpha mRNA level. The E(2)-induced increase in ERbeta transcript was not associated with increased ERbeta protein. E(2) increased ERbeta mRNA expression also in the presence of LPS, suggesting that inflammation-induced impairment of ERbeta signalling is rescued by estrogen.}},
  author       = {{Holm, Anders and Andersson, Kristina E and Nordström, Ina and Hellstrand, Per and Nilsson, Bengt-Olof}},
  issn         = {{1872-8057}},
  language     = {{eng}},
  pages        = {{8--13}},
  publisher    = {{Elsevier}},
  series       = {{Molecular and Cellular Endocrinology}},
  title        = {{Down-regulation of endothelial cell estrogen receptor expression by the inflammation promoter LPS.}},
  url          = {{http://dx.doi.org/10.1016/j.mce.2010.01.002}},
  doi          = {{10.1016/j.mce.2010.01.002}},
  volume       = {{319}},
  year         = {{2010}},
}