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      Detection of Connective Tissue Growth Factor in Subretinal Fluid following Retinal Detachment: Possible Contribution to Subretinal Scar Formation, Preliminary Results

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          Abstract

          Connective tissue growth factor (CTGF) has been shown to be substantially involved in various processes of fibrosis. Herein we report on the presence of CTGF in the subretinal fluid (SRF) of patients with retinal detachment. Methods: Samples of SRF were collected from 10 patients during retinal detachment surgery. Specific ELISA analysis was performed with goat IgG against human CTGF. Results: CTGF was above the detection limit of the assay in all samples. On average the concentration of CTGF in SRF was 10 ng/ml (SD 3.7, range 3.7–15.7 ng/ml). There was an increase in the CTGF concentration with time between the diagnosis of retinal detachment and surgery (correlation r = 0.67). Conclusion: CTGF appears to be a constant component of the fluid accumulating in the subretinal space after retinal detachment. The origin of subretinal CTGF and its physiological importance is still unclear. The known effects of CTGF, however, suggest that it may be involved in both the physiological processes of wound healing in the subretinal space and also in the pathological events such as subretinal fibrosis. The observed increase in CTGF concentration with time suggest that CTGF plays a role in the pathophysiology of subretinal scarring in cases of delayed retinal surgery.

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          Connective tissue growth factor: a cysteine-rich mitogen secreted by human vascular endothelial cells is related to the SRC-induced immediate early gene product CEF-10

          G Grotendorst, D. Bradham, H. Igarashi … (1991)
          Human umbilical vein endothelial (HUVE) cells have been previously reported to express the genes for the A and B chains of PDGF and to secrete PDGF-related factors into culture media. Antihuman PDGF IgG affinity chromatography was used to purify PDGF-related activity from HUVE cell-conditioned media. Immunoblot analysis of the affinity- purified proteins with anti-PDGF IgG and antibodies specific for the A or B chain peptides of PDGF combined with chemotactic and mitogenic assays revealed that the major PDGF immunorelated molecule secreted by HUVE cells is a monomer of approximately 36-38 kD and that less than 10% of the purified biologically active molecules are PDGF A or B chain peptides. Screening of an HUVE cell cDNA library in the expression vector lambda gtl 1 with the anti-PDGF antibody resulted in the cloning and sequencing of a cDNA with an open reading frame encoding a 38-kD cysteine-rich secreted protein which we show to be the major PDGF- related mitogen secreted by human vascular endothelial cells. The protein has a 45% overall homology to the translation product of the v- src-induced CEF-10 mRNA from chick embryo fibroblasts. We have termed this new mitogen connective tissue growth factor.
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            CTGF expression is induced by TGF- beta in cardiac fibroblasts and cardiac myocytes: a potential role in heart fibrosis.

            M. M. Chen, A. Lam, J A Abraham … (2000)
            Connective tissue growth factor (CTGF) is a cysteine-rich protein induced by transforming growth factor beta (TGF- beta) in connective tissue cells. CTGF can trigger many of the cellular processes underlying fibrosis, such as cell proliferation, adhesion, migration and the synthesis of extracellular matrix; however, its role in acute and chronic cardiac injury is not fully understood. Here, we show that TGF- beta is a specific inducer of CTGF expression in both cardiac fibroblasts and cardiac myocytes. The activity of a CTGF promoter-based reporter construct correlated with endogenous CTGF expression, suggesting that TGF- beta induces CTGF expression most likely by activating its promoter. Upregulation of CTGF coincided with an increase in fibronectin, collagen type I and plasminogen activator inhibitor-1 production. Forskolin, a stimulator of cyclic AMP, blocked TGF- beta induced CTGF expression and reduced the basal level of CTGF, whereas an inhibitor that blocks the MAP kinase signaling pathway (PD 98059) significantly enhanced TGF- beta induced CTGF expression. Furthermore, we found that both TGF- beta and CTGF mRNAs were significantly elevated in the left ventricles and septa of rat hearts 2-16 weeks following myocardial infarction. This correlated well with concomitant increases in fibronectin, and type I and type III collagen mRNA levels in these animal hearts. Significant upregulation of CTGF was also detected in human heart samples derived from patients diagnosed with cardiac ischemia. Based on these findings, we propose that CTGF is an important mediator of TGF- beta signaling in the heart and abnormal expression of this gene could be used as a diagnostic marker for cardiac fibrosis. Copyright 2000 Academic Press.
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              Müller cell and neuronal remodeling in retinal detachment and reattachment and their potential consequences for visual recovery: a review and reconsideration of recent data.

              Steven Fisher, Geoffrey Lewis (2003)
              Recent evidence suggests that the adult mammalian retina is far more plastic than was previously thought. Retinal detachment induces changes beyond the degeneration of outer segments (OS). Changes in photoreceptor synapses, second- and even third-order neurons may all contribute to imperfect visual recovery that can occur after successful reattachment. Changes that occur in Müller cells have obvious effects through subretinal fibrosis and proliferative vitreoretinopathy, but other unidentified effects seem likely as well. Reattachment of the retina induces its own set of responses aside from OS re-growth. Reattachment halts the growth of Müller cell processes into the subretinal space, but induces their growth on the vitreal surface. It also induces the outgrowth of rod axons into the inner retina.
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                Author and article information

                Journal
                Journal ID (publisher-id): ORE
                Journal ID (nlm-ta): Ophthalmic Res
                Journal ID (doi): 10.1159/issn.0030-3747
                Title: Ophthalmic Research
                Publisher: S. Karger AG
                ISSN (Print): 0030-3747
                ISSN (Electronic): 1423-0259
                Publication date Subscription-year: 2005
                Publication date (Print): December 2005
                Publication date (Electronic): 21 October 2005
                Volume: 37
                Issue: 6
                Pages: 289-292
                Affiliations
                aSt Eriks Eye Clinic, Karolinska Institutet, Stockholm, Sweden, and bDepartment of Obstetrics and Gynecology, Institute of Wound Healing, University of Florida, Gainesville, Fla., USA
                Article
                Publisher ID: 87698 Other ID: Ophthalmic Res 2005;37:289–292
                DOI: 10.1159/000087698
                PubMed ID: 16118511
                SO-VID: 80282256-77ff-4a6a-99ba-4c0a67e492d8
                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
                Page count
                Figures: 1, References: 22, Pages: 4
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Vision sciences,Ophthalmology & Optometry,Pathology
                Keywords: Connective tissue growth factor,Scarring,Apoptosis,Fibrosis,Retinal detachment,Receptors,Vascular endothelial growth factor,Wound healing
                Data availability:
                ScienceOpen disciplines: Vision sciences, Ophthalmology & Optometry, Pathology
                Keywords: Connective tissue growth factor, Scarring, Apoptosis, Fibrosis, Retinal detachment, Receptors, Vascular endothelial growth factor, Wound healing

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