Stable over-expression of estrogen receptor-α in ECV304 cells inhibits proliferation and levels of secreted endothelin-1 and vascular endothelial growth factor

Syed Hamid Ali, Amy L. O'Donnell, Seema Mohamed, Shakir Mousa, Paresh Dandona

Research output: Contribution to journalArticlepeer-review

21 Citations (Scopus)

Abstract

Studies with mammalian vascular cells have suggested growth inhibitory effects of estrogen on the vascular wall. To investigate the involvement of estrogen receptor-α (ER) in the control of endothelial cell proliferation, we have stably transfected human estrogen receptor-α cDNA into the endothelial cell line ECV304. The clone ECV-ER, thus obtained, over-expresses estrogen receptor to a level ~ 10-fold higher than the parent cell line. Effects of this over-expression were studied on the celt growth rate, and on the levels of secreted endothelin-1 and vascular endothelial growth factor (VEGF). Similar to the previously reported data in other cell types, we found the transfection of ER in ECV304 cells to be inhibitory to their growth. Our ER-over-expressing clone of ECV304 also showed an inhibition of secreted endothelin-1 and VEGF levels. Moreover, the growth inhibition of this ER- over-expressing clone was reversed by the addition of endothelin-1 or VEGF to the medium. In view of the growth-stimulatory effect of endothelin-1 and VEGF on vascular cells, our results indicate that estrogen receptor-α may bring about its growth inhibition partly by suppressing endothelin-1 and/or VEGF production in ECV304 cells.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalMolecular and Cellular Endocrinology
Volume152
Issue number1-2
DOIs
Publication statusPublished - Jun 25 1999

Keywords

  • Atherosclerosis
  • Cardiovascular disease
  • ECV304
  • Endothelial cells
  • Endothelin-1
  • Estrogen
  • Estrogen receptor-α
  • Growth behavior
  • Heart disease
  • Proliferation rate
  • Stable transfection
  • Vascular disease

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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