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      Inhibition of Fibroblast and Smooth Muscle Cell Proliferation and Migration in vitro by a Novel Aminochromone U-67154

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          Abstract

          Medial smooth muscle cell migration and neointimal proliferation are primary contributors to the delayed restenosis that occurs after percutaneous transluminal coronary angioplasty. In this study, we describe the antiproliferative and antichemotactic properties of U-67154, the parent compound of a series of novel aminochromones, determined using in vitro fibroblast and smooth muscle cell culture systems. U-67154 inhibited the induction of DNA synthesis in confluent BALB/c 3T3 fibroblasts and early-passage rat aortic smooth muscle cells by several different growth factors in a concentration-dependent manner. U-67154 similarly inhibited the proliferation of these cells stimulated by serum. Growth-factor-induced chemotaxis of fibroblasts and early-passage rat aortic smooth muscle cells also was inhibited by U-67154 in a concentration-dependent manner. The IC50S for all of these functions were similar (between 120 and 200 µM). Such antiproliferative and antichemotactic effects did not result from cytotoxicity (as measured by lactate dehydrogenase release, neutral red uptake or nonspecific inhibition of protein synthesis). Most important, inhibition of long-term proliferation of fibroblasts and early-passage smooth muscle cells by U-67154 was fully reversible upon removal of the drug. Thus, U-67154 represents a class of novel, noncytotoxic compounds that may prove useful in the treatment of proliferative disorders such as delayed restenosis after percutaneous transluminal coronary angioplasty.

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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
          1993
          1993
          23 September 2008
          : 30
          : 2
          : 108-115
          Affiliations
          aCardiovascular Diseases Research and bMedicinal Chemistry, Upjohn Laboratories, Kalamazoo, Mich. cLilly Research Laboratory, Indianapolis, Ind., USA
          Article
          158982 J Vasc Res 1993;30:108–115
          10.1159/000158982
          8267792
          © 1993 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
          Pages: 8
          Categories
          Research Paper

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