Estrogen receptor-α gene transfer into bovine aortic endothelial cells induces eNOS gene expression and inhibits cell migration

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Abstract
Objectives: It has been suggested that estrogen may improve endothelial cell function to delay the onset of atherosclerosis in pre-menopausal females, though its mechanism of action is not fully understood. We examined the hypothesis that human estrogen receptor-α (ERα) gene transfection improves the endothelial cell function. Methods: A replication deficient adenoviral vector was used to transfect the ERα gene into bovine aortic endothelial cells (BAEC) and a GFP gene containing vector was used as control. Expression of the eNOS gene was determined by Northern blot analysis and enzyme activity assay; cell migration was assayed using a Transwell apparatus; and tyrosine phosphorylation of FAK was estimated by Western blot analysis. Results: ERα gene transfection of endothelial cells produced a 2–3-fold increase in eNOS mRNA and protein levels as well as a significant increase (PPConclusion: Our results suggest that the atheroprotective effects of estrogen may in part be mediated by ERα-induced upregulation of eNOS gene expression and maintenance of endothelial cell function and integrity.

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