Role of estrogen receptor on αVβ3-mediated cell adhesion, migration and secretion of bFGF and VEGF in human endothelial and endometrial cells

S. Mohamed, S. Ali, P. Dandona, S. A. Mousa

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Cell adhesion molecules, production of chemotactic factors and elevated level of growth factors are involved in angiogenesis leading to cancer growth, metastasis, atherosclerosis and endometriosis. In this study, we have measured cell adhesion, migration and secretion of b-FGF and VEGF. ER transfected cells were maintained in phenol red free growth medium supplemented with charcoal /dextran stripped fetal bovine serum. Serum free growth medium was used in experiments. ER transfected ECV and Ishikawa cells demonstrated an αVβ3-mediated upregulation of cell adhesion to fibrinogen and osteopontin (OPN) matrix proteins but not to fibronectin or vitronectin. Similar to the αVβ3 monoclonal antibody LM609 (1.25 ug/ml), b-estradiol (0.01 μM) decreased αVβ3-mediated cell adhesion to either fibrinogen or osteopontin. Additionally, estrogen decreased the migration of both control and ER transfected ECV cells towards VN and OPN matrix proteins after 18 hours. Whereas Ishikawa cells demonstrated very little or no migration after 96 hours. ER transfected cells secreted significantly more VEGF and b-FGF as compared to respective control. These data suggests a differential upregulation of αVβ3 integrin by estrogen and ER in human endothelial and endometrium cells.

Original languageEnglish
Pages (from-to)A771
JournalFASEB Journal
Volume12
Issue number5
Publication statusPublished - Mar 20 1998
Externally publishedYes

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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