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      Expression and Function of Recombinant Endothelial Nitric Oxide Synthase in Human Endothelial Cells

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          Endothelial dysfunction is frequently involved in the pathogenesis of vascular disease. While nitric oxide (NO) inhibits smooth muscle cell proliferation, its effect on endothelial cell proliferation is unclear. The aim of this study was to determine if adenoviral-mediated gene transfer of endothelial NO synthase (eNOS) to human umbilical vein endothelial cells (HUVECs) would result in increased generation of NO and affect endothelial cell proliferation. HUVECs were transduced with adenoviral vectors encoding eNOS (AdeNOS) or β-galactosidase (Adβgal) or exposed to diluent (control). AdeNOS-transduced cells showed increased eNOS expression as detected by Western blot analysis, and increased concentrations of cGMP (control 0.7 ± 0.1; Adβgal 0.9 ± 0.2; AdeNOS 3.1 ± 0.5 pmol/mg protein; p < 0.001) and nitrite (control 11.8 ± 1.2; Adβgal 13.3 ± 1.7; AdeNOS 21.1 ± 2.2 nmol/mg protein/hour; p < 0.01). DNA synthesis as assessed by [<sup>3</sup>H]thymidine incorporation and cell counts were significantly reduced (by ∼30%) in AdeNOS-transduced HUVECs. Expression of mitogen-activated protein kinase was also decreased in AdeNOS-transduced cells. This study shows that adenoviral-mediated gene transfer of eNOS to HUVECs inhibits endothelial cell proliferation.

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          Exogenous nitric oxide inhibits proliferation of cultured vascular endothelial cells.

           J Ando,  A Kamiya,  Wei Yang (1994)
          Cultured bovine fatal aortic endothelial cells (BAECs) were stimulated with nitric oxide (NO)-releasing vasodilators and NO gas-saturated solution, and changes in the cell proliferation were examined. Sodium nitroprusside (SNP) and nitroglycerin (NTG) shifted the growth curve downward, and inhibited 3H-thymidine incorporation by the ECs in a dose-dependent manner. Application of NO solution also reduced 3H-thymidine incorporation. SNP, NTG and NO solution increased the intracellular cGMP in BAECs. A cGMP analog, 8-bromo-cGMP, inhibited 3H-thymidine incorporation, and a guanylate cyclase inhibitor, methylene blue, almost completely blocked the inhibitory effect of SNP and NTG on 3H-thymidine incorporation. These findings suggest that exogenous NO inhibits EC proliferation, and that intracellular cGMP is involved in the inhibitory effect of NO.

            Author and article information

            J Vasc Res
            Journal of Vascular Research
            S. Karger AG
            December 2000
            10 January 2001
            : 37
            : 6
            : 449-456
            Departments of aEndocrinology and bAnesthesiology, Mayo Clinic and Foundation, Rochester, Minn., USA
            54077 J Vasc Res 2000;37:449–456
            © 2000 S. Karger AG, Basel

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            Page count
            Figures: 8, References: 27, Pages: 8
            Research Paper


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