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      Serum Matrix Metalloproteinases MMP-2 and MMP-3 Levels in Dialysis Patients Vary Independently of CRP and IL-6 Levels

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          Abstract

          Background: Patients on chronic hemodialysis or peritoneal dialysis often develop an inflammatory state that causes morbidity and mortality. Cross-sectional studies of dialysis patients have determined that C-reactive protein (CRP) is a predictor of morbidity. Little is known as to whether CRP, cytokines, such as IL-6 and IL-1β that stimulate the synthesis of CRP, or matrix metalloproteinases (MMPs) are markers of inflammation in patients on dialysis. Methods: We assayed by ELISA serum levels of MMP-2, MMP-3, IL-6 and CRP in healthy individuals and in patients with pre-end-stage renal disease (pESRD, n = 10), peritoneal dialysis (PD, n = 11), hemodialysis (HD, n = 17) and renal transplant (TX, n = 10). Results: MMP-2 was significantly elevated before dialysis, perhaps indicative of progressive chronic renal sclerosis. MMP-3 was markedly elevated in hemodialysis patients but not in pESRD or PD patients, and may be related to the hemodialysis process and/or accelerated atherogenesis in these patients. IL-6 was significantly elevated in all patient groups, including pESRD patients. There were no statistically significant differences in CRP levels among the study groups. CRP correlated with IL-6, but not with MMP-2 or MMP-3. Conclusions: The data indicate that there are measurable differences in the expression of MMPs within the dialysis patient population. Because dialysis can be associated with local and systemic inflammation, increased levels of MMP-3 in the hemodialyis group may be a reflection of gene stimulation induced by inflammatory cytokines and should be considered as a marker of chronic, local inflammation.

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          Most cited references 3

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          Increased matrix metalloproteinase-3 serum levels in rheumatic diseases: relationship with synovitis and steroid treatment.

          To determine matrix metalloproteinase-3 (MMP-3) serum levels in patients with rheumatic diseases and to study the relation between MMP-3 and C reactive protein (CRP) levels. MMP-3 serum levels were determined by enzyme linked immunosorbent assay (ELISA) in (a) patients with active inflammatory rheumatic diseases: rheumatoid arthritis (RA), psoriatic arthritis, polymyalgia rheumatica, acute crystal arthritis, and ankylosing spondylitis; (b) patients with active inflammatory systemic diseases: cutaneo-articular or renal systemic lupus erythematosus (SLE), systemic sclerosis, and vasculitides; (c) patients with non-inflammatory rheumatic diseases: osteoarthritis and fibromyalgia; (d) critically ill patients without rheumatic diseases, representing an acute inflammatory control group; (e) healthy controls. MMP-3 serum levels were significantly increased in patients with active RA, psoriatic arthritis, and polymyalgia rheumatica, whether treated or not by corticosteroids, and in female patients with acute crystal arthritis. MMP-3 serum levels were normal in steroid-free patients with active cutaneo-articular or renal SLE, systemic sclerosis, and vasculitides but were significantly increased in steroid treated patients. MMP-3 levels were normal in fibromyalgia, osteoarthritis, ankylosing spondylitis, and acute inflammatory controls. MMP-3 was significantly correlated with CRP in RA (r=0.5, p=0.0004) but not in any of the other disease groups. MMP-3 serum levels are increased in inflammatory rheumatic diseases characterised by joint synovitis, such as RA, polymyalgia rheumatica, psoriatic arthritis, and acute crystal arthritis-that is, whether the diseases are acute or chronic, erosive or not. They are normal in SLE, systemic sclerosis, and vasculitides as well as in non-rheumatic inflammatory controls, but are significantly increased by steroids. These data strongly suggest that serum MMP-3 reflects synovial inflammation.
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            Matrix metalloproteinase 2 (gelatinase A) regulates glomerular mesangial cell proliferation and differentiation.

             J Turck,  Hugo Marti,  L. Lee (1996)
            A biologic role for the 72-kDa gelatinase A (matrix metalloproteinase 2; MMP-2), beyond simple extracellular matrix turnover, was evaluated in glomerular mesangial cells. To determine the significance of MMP-2 secretion for the acquisition of the inflammatory phenotype, we reduced the constitutive secretion of MMP-2 by cultured mesangial cells with antisense RNA expressed by an episomally replicating vector or with specific anti-MMP-2 ribozymes expressed by a retroviral transducing vector. The phenotype of the transfected, or retrovirally infected, cells was profoundly altered from the activated state and closely approximated that of quiescent cells in vivo. The prominent differences included a change in the synthesis and organization of the extracellular matrix, loss of activation markers, and a virtually total exit from the cell cycle. Reconstitution with exogenous active, but not latent MMP-2, induced a rapid return to the inflammatory phenotype in vitro. This effect was specific to MMP-2, because the closely related MMP-9 did not reproduce these changes. Furthermore, this pro-inflammatory effect of MMP-2 is dependent upon the active form of the enzyme, which can be produced by an autocatalytic activation process on the mesangial cell plasma membrane. It is concluded that MMP-2 acts directly upon mesangial cells to permit the development of an inflammatory phenotype. Specific inhibition of MMP-2 activity in vivo may represent an alternate means of ameliorating complex inflammatory processes by affecting the phenotype of the synthesizing cells, per se.
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              Hepatocellular Dysfunction after Severe Hypotension in the Absence of Blood Loss Is Associated with the Increased IL-6 and PGE2

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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2002
                October 2002
                18 October 2002
                : 92
                : 4
                : 817-823
                Affiliations
                Division of Nephrology and Hypertension, Department of Medicine, and Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, N.C., USA
                Article
                65464 Nephron 2002;92:817–823
                10.1159/000065464
                12399626
                © 2002 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: 4, Tables: 2, References: 39, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/65464
                Categories
                Original Paper

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