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

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          Abstract

          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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          Most cited references 1

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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.
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            Author and article information

            Journal
            JVR
            J Vasc Res
            10.1159/issn.1018-1172
            Journal of Vascular Research
            S. Karger AG
            1018-1172
            1423-0135
            2000
            December 2000
            10 January 2001
            : 37
            : 6
            : 449-456
            Affiliations
            Departments of aEndocrinology and bAnesthesiology, Mayo Clinic and Foundation, Rochester, Minn., USA
            Article
            54077 J Vasc Res 2000;37:449–456
            10.1159/000054077
            11146398
            © 2000 S. Karger AG, Basel

            Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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

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