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      Smooth Muscle Cell Outgrowth from Coronary Atherectomy Specimens in vitro Is Associated with Less Time to Restenosis and Expression of a Key Transcription Factor KLF5/BTEB2

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          Abstract

          Atherectomy specimens offer an opportunity to study the biology of coronary artery lesions. We cultured smooth muscle cells (SMCs) from specimens obtained from 24 patients with coronary restenosis after angioplasty to study the relationship between activity of SMCs (in vitro outgrowth) and the time course of restenosis. We also examined expression of a Kruppel-like zinc-finger transcription factor 5 (KLF; also known as BTEB2 and IKLF), which is markedly induced in activated SMCs, in the same specimens. SMC outgrowth was observed in 9 of 24 specimens (37.5%). Restenosis occurred sooner (p < 0.01) in patients whose specimens showed outgrowth compared to those whose specimens showed no outgrowth. Immunostaining for KLF5 was more common in specimens with outgrowth (89 vs. 20%, p < 0.01). These data suggest that the number of activated SMCs in lesions may determine in vitro outgrowth and also affect the time to restenosis.

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          Restenosis after percutaneous transluminal coronary angioplasty: have we been aiming at the wrong target?

          Jesse W. Currier, David Faxon (1995)
          Restenosis after percutaneous coronary balloon angioplasty remains a significant problem. Despite success with a variety of agents in animal models, no agent has proved clearly successful in reducing restenosis in humans. There are many potential reasons for this, but one possibility is that because of our incomplete understanding of the restenotic process, therapy has been directed at the wrong target. Arterial remodeling (changes in total vessel area or changes in area circumscribed by the internal elastic lamina) is well described in de novo atherosclerosis, and there is increasing evidence that this process occurs after angioplasty. Thus, restenosis can be thought of not merely as neointimal formation in response to balloon injury, but as arterial remodeling in response to balloon injury and neointimal formation. Arterial remodeling may consist of actual constriction of the artery, as has been described in some animal models and in preliminary fashion in humans, or of compensatory enlargement as has been described in de novo atherosclerosis and in the hypercholesterolemic rabbit iliac artery model. Arterial constriction can result in restenosis with minimal neointimal formation. Compensatory enlargement accommodates significant amounts of neointimal formation, with preservation of lumen area despite an increase in neointimal area adequate to cause restenosis in a noncompensated artery. This expanded paradigm of arterial remodeling and intimal formation may in part account for the lack of success in clinical trials to date, and therapy directed at arterial remodeling as well as intimal formation may be required to reduce restenosis after coronary interventions.
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            Relation between Activated Smooth-Muscle Cells in Coronary-Artery Lesions and Restenosis after Atherectomy

            Michael Simons, Guy Leclerc, Robert D Safian … (1993)
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              Analysis of atherectomy specimens

              Berthold Höfling, Ulrich Welsch, Jürgen Heimerl … (1993)
              Article 0 comments Cited 5 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): CRD
                Journal ID (nlm-ta): Cardiology
                Journal ID (doi): 10.1159/issn.0008-6312
                Title: Cardiology
                Publisher: S. Karger AG
                ISSN (Print): 0008-6312
                ISSN (Electronic): 1421-9751
                Publication date Subscription-year: 2003
                Publication date (Print): October 2003
                Publication date (Electronic): 17 October 2003
                Volume: 100
                Issue: 2
                Pages: 80-85
                Affiliations
                Departments of aGeneral Medicine and bMedical Informatics, and cSecond Department of Internal Medicine, Gunma University School of Medicine, Maebashi, and dDepartment of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
                Article
                Publisher ID: 73043 Other ID: Cardiology 2003;100:80–85
                DOI: 10.1159/000073043
                PubMed ID: 14557694
                SO-VID: 20758227-84ee-46a2-a0ae-4f7f278ba78d
                Copyright © © 2003 S. Karger AG, Basel
                License:

                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.

                History
                Date received : 21 February 2003
                Date accepted : 30 June 2003
                Page count
                Figures: 3, Tables: 2, References: 26, Pages: 6
                Categories
                Subject: General Cardiology – Basic Science

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: KLF5,Cell culture,Transcription factor,Restenosis,Atherectomy,Smooth muscle cell
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: KLF5, Cell culture, Transcription factor, Restenosis, Atherectomy, Smooth muscle cell

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