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      Sublytic Complement Injury Does Not Activate NF-κB, or Induce Mitogenesis in Rat Mesangial Cells

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          Abstract

          Sublytic complement injury to glomerular mesangial cells, mediated by the terminal membrane attack complex of complement (C5b-9), is a potential initiating mechanism in IgA nephropathy. Sublytic complement injury has been reported to result in the production of a variety of pro-inflammatory molecules and growth factors, including many regulated by the transcription factor NF-κB. To determine the importance of complement injury in the pro-inflammatory signalling which occurs in IgA nephropathy, we investigated NF-κB activation following sublytic complement injury to cultured rat glomerular mesangial cells (RMCs). A sublytic dose of rabbit anti-Thy 1.1 (THY) serum and normal human serum was selected based upon flow cytometry, chromium-release assay, and induction of superoxide production. No significant C5b-9-induced NF-κB activation was detected by electrophoretic mobility shift assays, luciferase activity of RMCs transfected with a NF-κB-driven luciferase reporter construct, nor by Northern blots for the NF-κB-responsive mRNA species monocyte chemoattractant protein-1 or IκBα. Furthermore, measurements of <sup>3</sup>H incorporation following sublytic complement injury showed inhibition of mesangial cell mitogenesis in comparison to the heat-inactivated serum treatment and to THY alone. The results of this study suggest that sublytic complement injury to RMC does not directly activate NF-κB nor induce mesangial cell proliferation in mesangial cells. Other mechanisms such as IgA immune complex formation must be required to produce these events in IgA nephropathy.

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          Author and article information

          Journal
          EXN
          Nephron Exp Nephrol
          10.1159/issn.1660-2129
          Cardiorenal Medicine
          S. Karger AG
          1660-2129
          2000
          October 2000
          31 July 2000
          : 8
          : 4-5
          : 291-298
          Affiliations
          Immunology Research Centre, St. Vincent’s Hospital, Melbourne, Australia
          Article
          20681 Exp Nephrol 2000;8:291–298
          10.1159/000020681
          10940729
          © 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: 5, References: 26, Pages: 8
          Product
          Self URI (application/pdf): https://www.karger.com/Article/Pdf/20681
          Categories
          Original Paper

          Cardiovascular Medicine, Nephrology

          Mitogenesis, Mesangial cell, NF-ĸB, Complement, Sublytic

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