Effects of estrogen on nitric oxide synthase expression in rat aorta allograft and smooth muscle cells.

Background: We find that chronic estradiol treatment inhibits the development of transplant arteriosclerosis (TA). The mechanism of this inhibition remains unclear. The objective of this study is to investigate in a non-cyclosporin-requiring TA model whether estradiol-17beta treatment modulates the expression of both endothelial nitric oxide synthase (ecNOS) and inducible nitric oxide synthase (iNOS) in the early phase following transplantation.

Growth and phenotypic characterization of porcine coronary artery smooth muscle cells.

Vascular smooth muscle cell (VSMC) proliferation significantly contributes to atherosclerotic plaque formation and limits the success rate of percutaneous transluminal coronary angioplasty. We derived a population of porcine coronary artery SMCs to characterize VSMC proliferation and phenotype in preparation to study the molecular actions of VSMC mitogens and antiproliferative agents. Growth assays were designed to minimize the estrogen content in the culture medium, since this steroid hormone significantly influences VSMC growth and the expression of VSMC mitogens and their receptors.

Inhibition of estrogen receptor function promotes porcine coronary artery smooth muscle cell proliferation.

Estradiol-17beta (E2) can inhibit vascular smooth muscle cell (VSMC) proliferation probably through its ability to activate its nuclear estrogen receptors (ER). Activation or inhibition of the ER by cognate permissive or non-permissive ligands, respectively, would indicate whether ER action is critical for this vascular protective effect. We investigated a previously characterized population of cultured porcine coronary artery SMCs for ER expression and for the response of these cells to estrogens and antiestrogens.

Oestrogen and transplant vascular disease.

1. The aetiology of chronic rejection is clearly multifactorial and relates to both immunological and non-immunological factors. 2.