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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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          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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          Most cited references 16

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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

          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.

            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.

              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.

                Author and article information

                Ophthalmic Res
                Ophthalmic Research
                S. Karger AG
                December 2005
                21 October 2005
                : 37
                : 6
                : 289-292
                aSt Eriks Eye Clinic, Karolinska Institutet, Stockholm, Sweden, and bDepartment of Obstetrics and Gynecology, Institute of Wound Healing, University of Florida, Gainesville, Fla., USA
                87698 Ophthalmic Res 2005;37:289–292
                © 2005 S. Karger AG, Basel

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                Figures: 1, References: 22, Pages: 4
                Original Paper


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