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      Eicosapentaenoic Acid Inhibits Mitogen-Induced Endothelin-1 Production and DNA Synthesis in Cultured Bovine Mesangial Cells

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          Abstract

          The present study was designed to examine whether eicosapentaenoic acid (EPA) inhibits the production of basal or stimulated endothelin (ET)-1 by platelet-derived growth factor (PDGF)-BB or epidermal growth factor (EGF), and DNA synthesis in cultured bovine mesangial cells. PDGF-BB and EGF stimulated ET-1 secretion in a dose-dependent fashion in these cells. EPA (10–100 µ M) exhibited dose-related inhibition of PDGF-BB- and EGF-stimulated ET-1 secretion. EPA had no inhibitory effects on basal ET-1 secretion in these cells. Moreover, 50 µ M EPA significantly attenuated PDGF-BB- and EGF-stimulated [<sup>3</sup>H]thymidine incorporation into mesangial cells. Receptor-binding experiments showed that EPA competitively inhibited <sup>125</sup>I-PDGF-BB or <sup>125</sup>I-EGF binding to mesangial cell surface receptors. Scatchard analysis for PDGF-BB receptor or EGF receptor revealed a linear regression fit and one binding site. Pretreatment with 50 µ M EPA suppressed the number of maximum binding sites, but did not affect the K<sub>d</sub> values. These results indicate that EPA potentially inhibits mesangial cell ET-1 production, when stimulated by PDGF-BB or EGF. This inhibitory effect of EPA could be related to the attenuation of mesangial cell proliferation via inhibition of the binding of PDGF-BB or EGF to their receptors due to alteration of the physicochemical characteristics of the cell membrane.

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          Author and article information

          Journal
          AJN
          Am J Nephrol
          10.1159/issn.0250-8095
          American Journal of Nephrology
          S. Karger AG
          0250-8095
          1421-9670
          1998
          April 1998
          01 April 1998
          : 18
          : 2
          : 164-170
          Affiliations
          Department of Medicine, Kidney Center, Tokyo Women’s Medical College, Tokyo, Japan
          Article
          13328 Am J Nephrol 1998;18:164–170
          10.1159/000013328
          9569962
          © 1998 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: 7, Tables: 1, References: 31, Pages: 7
          Product
          Self URI (application/pdf): https://www.karger.com/Article/Pdf/13328
          Categories
          Laboratory Investigation

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