For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
21
views
24
references
 Top references
cited by
1
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      269
      similar
       All similar

      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found

      Suppressive Effects of Iron on TGF-β 1 Production by Renal Proximal Tubular Epithelial Cells

      research-article

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background: TGF-β<sub>1</sub>, which is one of the profibrogenic cytokines, is considered essential for both the tubulointerstitial fibrosis found in chronic kidney diseases and the repair of tissue damage in acute renal injury. Iron plays an important part in inflammatory damage since it supplies cytotoxic hydroxyl radicals. The aim of the present study was to examine the direct effects of iron on TGF-β<sub>1</sub> production and the expression of 8-hydroxy-2′-deoxyguanosine (8-OHdG), a marker of oxidative stress, by human renal proximal tubular epithelial cells (RPTEC). Methods: Using human RPTEC, TGF-β<sub>1</sub> expression was studied by immunohistochemical staining, ELISA and RNase protection assays. 8-OHdG expression was evaluated by immunohistochemical staining. Results: Ferric iron suppressed both TGF-β<sub>1</sub> secretion and mRNA expression, and enhanced 8-OHdG expression in RPTEC in a dose-dependent manner. Desferrioxamine, an iron chelator, eliminated the suppressive effect of ferric citrate on TGF-β<sub>1</sub> production. Conclusions: The results suggest that iron may delay the repair of kidney injury during the acute inflammatory phase via a reduction in TGF-β<sub>1</sub> production by RPTEC. Iron chelation may therefore be a useful strategy in the treatment of inflammatory kidney diseases.

          Related collections

          Most cited references24

          • Record: found
          • Abstract: not found
          • Article: not found

          Transforming growth factor beta in tissue fibrosis.

          W Border, N Noble (1994)
          Article 0 comments Cited 486 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Pathophysiology of progressive nephropathies.

            G. Remuzzi, T Bertani (1998)
            Article 0 comments Cited 180 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-beta antibody in db/db diabetic mice.

              F Ziyadeh, B. B. Hoffman, D Han … (2000)
              Emerging evidence suggests that transforming growth factor-beta (TGF-beta) is an important mediator of diabetic nephropathy. We showed previously that short-term treatment with a neutralizing monoclonal anti-TGF-beta antibody (alphaT) in streptozotocin-diabetic mice prevents early changes of renal hypertrophy and increased matrix mRNA. To establish that overactivity of the renal TGF-beta system mediates the functional and structural changes of the more advanced stages of nephropathy, we tested whether chronic administration of alphaT prevents renal insufficiency and glomerulosclerosis in the db/db mouse, a model of type 2 diabetes that develops overt nephropathy. Diabetic db/db mice and nondiabetic db/m littermates were treated intraperitoneally with alphaT or control IgG, 300 microgram three times per week for 8 wk. Treatment with alphaT, but not with IgG, significantly decreased the plasma TGF-beta1 concentration without decreasing the plasma glucose concentration. The IgG-treated db/db mice developed albuminuria, renal insufficiency, and glomerular mesangial matrix expansion associated with increased renal mRNAs encoding alpha1(IV) collagen and fibronectin. On the other hand, treatment with alphaT completely prevented the increase in plasma creatinine concentration, the decrease in urinary creatinine clearance, and the expansion of mesangial matrix in db/db mice. The increase in renal matrix mRNAs was substantially attenuated, but the excretion of urinary albumin factored for creatinine clearance was not significantly affected by alphaT treatment. We conclude that chronic inhibition of the biologic actions of TGF-beta with a neutralizing monoclonal antibody in db/db mice prevents the glomerulosclerosis and renal insufficiency resulting from type 2 diabetes.
              Article 0 comments Cited 165 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (publisher-id): NEE
                Journal ID (nlm-ta): Nephron Exp Nephrol
                Journal ID (doi): 10.1159/issn.1660-2129
                Title: Cardiorenal Medicine
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2129
                Publication date Subscription-year: 2005
                Publication date (Print): May 2005
                Publication date (Electronic): 03 March 2005
                Volume: 100
                Issue: 1
                Pages: e1-e10
                Affiliations
                aDepartment of Endocrinology, Metabolism and Nephrology, and bDepartment of Tumor Pathology, Kochi Medical School, Nankoku, Japan
                Article
                Publisher ID: 84107 Other ID: Nephron Exp Nephrol 2005;100:e1–e10
                DOI: 10.1159/000084107
                PubMed ID: 15731565
                SO-VID: 3b572630-18e3-42e7-9c73-3b1991a7ffcd
                Copyright © © 2005 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 : 31 March 2004
                Date accepted : 17 August 2004
                Page count
                Figures: 8, References: 40, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: 8-OHdG,Hematuria,Oxidative stress,Tubulointerstitial fibrosis,Proteinuria,Cytokine
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: 8-OHdG, Hematuria, Oxidative stress, Tubulointerstitial fibrosis, Proteinuria, Cytokine

                Comments

                Comment on this article