The cardioprotective effect of estrogen may be linked to endothelial cell-extracellular matrix (ECM) interactions that bind growth factors and anchor cells to the vessel wall. We determined the effect of ECM proteins and estradiol (E2) on HCAEC release of bFGF. Female HCAEC were grown to confluence in estrogen-depleted medium for 48 hr, and replated onto plastic culture dishes coated with ECM proteins. The cells were then treated for 2 hr with E2 (5 nM). The medium was replaced with serum-free medium. Conditioned media and cell layers were harvested separately, and evaluated by ELISA and immunoblot for bFGF. There were no changes in cell layer bFGF content for any experimental conditions. Release of bFGF into conditioned media was enhanced by E2 on type IV collagen, laminin, and fibronectin, by 429%, 216%, and 219%, respectively. HCAEC cultured on type 1 collagen did not release more bFGF. Heparin (5μg/ml) further enhanced E2-stimulated bFGF release. The estrogen receptor antagonist, ICI 182,780, significantly decreased bFGF release in the presence of E2 ± heparin. These data show that E2 specifically enhances bFGF release by HCAEC cultured on basement membrane proteins. This mechanism could contribute to the cardioprotective effects of estrogen.
|Original language||English (US)|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology