Thrombospondin: A New Attachment Protein in Preretinal Traction Membranes

Weller, Michael; Esser, Peter; Bresgen, M; Heimann, Klaus; Wiedemann, Peter

doi:10.1177/112067219200200103

Cited by 11 publications

(7 citation statements)

References 28 publications

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“…Preretinal membrane ECM has been shown to contain Types I, 11,111, and V collagen, tenascin, decorin, thrombospondin, fibronectin, with Type iV collagen, vitronectin, and laminin in microvessel BMs (Casaroli Marano et al, 1995;Hagedoni et al, 1993;Hosoda et al, 1992;Weller et al, 1992;Immonen et al, 1991;Scheiffarth et al, 1988;. In our study, most of the above components and, in addition, perlecan, bamacan, Types VI, VIII, XII, and XIV collagen were found in preretinal membranes (Figures 3a and 4; Table 1).…”

Section: Preretinal Membranes In Pdrmentioning

confidence: 97%

“…The membranes often grow on the retinal surface inside the vitreous (preretinally) and are vascularized accumulations of ECM and different cell types (Walshe et al, 1992;Ohira and de Juan, 1990;Sramek et al, 1989;Nork et al, 1987;. A fibrogenic cytokine, transforming growth factor-p ('KED), has been implicated in their formation (Hagedorn et al, 1993;Weller et al, 1992).…”

Section: Introductionmentioning

confidence: 98%

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Basement membrane abnormalities in human eyes with diabetic retinopathy.

Ljubimov¹,

Burgeson²,

Butkowski³

et al. 1996

J Histochem Cytochem.

150

100

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Vascular and parenchymal basement membranes (BMs) are thickened in diabetes, but alterations in individual BM components in diabetic eyes, especially in diabetic retinopathy (DR), are obscure. To identify abnormalities in the distribution of specific constituents, we analyzed cryostat sections of human eyes obtained at autopsy (seven normal, five diabetic without DR, and 13 diabetic with DR) by immunofluorescence with antibodies to 30 BM and extracellular matrix components. In non-DR eyes, no qualitative changes of ocular BM components were seen. In some DR corneas, epithelial BM was stained discontinuously for laminin-1, entactin/nidogen, and alpha3-alpha4 Type IV collagen, in contrast to non-DR corneas. Major BM alterations were found in DR retinas compared to normals and non-DR diabetics. The inner limiting membrane (retinal BM) of DR eyes had accumulations of fibronectin (including cellular) and Types I, III, IV (alpha1-alpha2), and V collagen. The BM zone of new retinal blood vessels in neovascularized areas accumulated tenascin and Type XII collagen, whereas normal, diabetic, and adjacent DR retinas showed only weak and irregular staining. In preretinal membranes, perlecan, bamacan, and Types VI, VIII, XII, and XIV collagen were newly identified. Diabetic BM thickening appears to involve qualitative alterations of specific BM markers at an advanced disease stage, with the appearance of DR.

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Section: Preretinal Membranes In Pdrmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

Basement membrane abnormalities in human eyes with diabetic retinopathy.

Ljubimov¹,

Burgeson²,

Butkowski³

et al. 1996

J Histochem Cytochem.

150

100

View full text Add to dashboard Cite

show abstract

“…The expression of TSP-1 is up-regulated in the ischemic and diabetic retina [25,26,27]. TSP-1 is present in preretinal fibrovascular membranes from patients with PDR and is assumed to be involved in extracellular matrix remodeling [28,29]. Laser photocoagulation, the presently most successful treatment of diabetic retinopathy [30], induces expression of TSP-1 in the murine retina [31].…”

Section: Introductionmentioning

confidence: 99%

Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Yafai¹,

Eichler²,

Iandiev³

et al. 2014

Ophthalmic Res

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Background/Aims: By the release of antiangiogenic factors, Müller glial cells provide an angiostatic environment in the normal and ischemic retina. We determined whether Müller cells produce thrombospondin-1 (TSP-1), a known inhibitor of angiogenesis. Methods: Secretion of TSP-1 by cultured Müller cells was determined with ELISA. Slices of rat retinas and surgically excised retinal membranes of human subjects were immunostained against TSP-1 and the glial marker vimentin. The effects of TSP-1 on the growth of bovine retinal endothelial cells (BRECs) and activation of ERK1/2 were determined with DNA synthesis and migration assays, and Western blotting, respectively. Results: Cultured Müller cells secrete TSP-1 under normoxic and hypoxic (0.2% O₂) conditions. Secretion of TSP-1 was increased in hypoxia compared to normoxia. In rat retinal slices, glial, retinal ganglion, and possibly horizontal cells were stained for TSP-1. Retinal glial cells in preretinal membranes from human subjects with nonhypoxic epiretinal gliosis (macular pucker) and proliferative diabetic retinopathy, respectively, were immunopositive for TSP-1. Exogenous TSP-1 reduced the VEGF-induced proliferation and migration of BRECs and decreased the phosphorylation level of ERK1/2 in BRECs. Conclusion: The data suggest that Müller cells are one major source of TSP-1 in the normal and ischemic retina. Glia-derived TSP1 may inhibit angiogenic responses in the ischemic retina.

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“…A missense mutation (N333S) in the TG2 gene active site has been found in Italians with maturity onset diabetes of the young [108]. Factor XIII and fibronectin have been found in preretinal membranes in diabetic retinopathy, suggesting a role for TG, at least in the advance stages of this disease [100].…”

Section: J Clinic Experiments Ophthalmolmentioning

confidence: 99%

“…In contrast, in a non-ocular context, the 110 kDa cell binding fragment of fibronectin has been shown to interact with cell surface integrins (namely the α1 β5 integrins) via TG2 [99] (Figure 3). c. Role of factor XIII in proliferative vitreoretinopathy: Colocalisation of blood coagulation factor XIII, a plasma TG and two of its substrates thrombospondin and fibronectin were observed in PVR [100]. Factor XIII is the crosslinking enzyme that stabilizes blood clot in the final stages of the blood coagulation cascade.…”

Section: B Role Of Transglutaminse-2 In Proliferative Vitreoretinopamentioning

confidence: 99%

Recent Advances: Transglutaminase in Ocular Health and Pathological Processes

Lan¹

2011

J Clin Exp Ophthalmol

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propelled further research in this field, and a wide variety of techniques have been employed, including peptides [14], small molecules [15], molecules from bacteria [16] and lead compounds discovered by screening [17]. (Figure 1) summarises the ocular disease states that have been linked to TG.Many abbreviations and synonyms of various types of TG have been used in the literature. For example, TG2 will be used in place of commonly encountered abbreviations such as 'TGc' and 'tTG'. Ocular Surface DiseasesStudies that linked TG to ocular surface diseases such as pterygium [18], allergic conjunctivitis [19], dry eye [20] and cicatricial conjunctivitis [21,22] have been performed, and will be described in the following sections. In the cornea and conjunctiva, TG activity can be detected in the intercellular spaces, along the basement membranes, the cytoplasm of the epithelial cells, the superficial stromal keratocytes, as well as in the walls of the conjunctival stromal vessels [4]. Although TG2 can be found within various ocular cell types, TG1 was identified only in the suprabasal layer of the corneal epithelium. AbstractTransglutaminase (TG) is a diverse class of crosslinking enzymes involved in the regulation of cytokine production, endocytosis, cell adhesion, migration, apoptosis and autophagy. It has been implicated in inflammatory diseases, neurodegenerative processes and cancer. The eye is a specialized organ which subserves the important function of vision and has distinctive physiological and anatomical properties that differ from other body tissues. Understanding of the roles of various TGs in the eye therefore require studies specific to cells and tissues of ocular origin. We review the advances in TG research in ocular diseases, including pterygium, glaucoma, cataract and proliferative vitreoretinopathy. TG1 is a molecule important for keratinisation in many cicatrizing diseases of the ocular surface, including keratoconjunctivitis sicca. TG2, with multiple functions, has been shown to be important in inflammation and cell adhesion in various ocular diseases. The results of TG research in each region of the eye are critically assessed and the implications of these studies in the treatment of ocular diseases are discussed. By modifying wound healing process and influencing the amount of inflammation in animal models of human ocular diseases, TG-related strategies are now a possibility for selected clinical scenarios. For example, the use of retinoic acid for severe dry eye has undergone clinical trials. However, in many other areas, more research in selection of specific targets, time of intervention, specific method of delivery of interventional molecules, and safety of therapy in humans may be necessary. One promising area in the future is the use of a TG strategy to modify conjunctival wound healing to increase success rates after glaucoma surgery.

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Thrombospondin: A New Attachment Protein in Preretinal Traction Membranes

Cited by 11 publications

References 28 publications

Basement membrane abnormalities in human eyes with diabetic retinopathy.

Basement membrane abnormalities in human eyes with diabetic retinopathy.

Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Recent Advances: Transglutaminase in Ocular Health and Pathological Processes

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