Vitronectin and proliferative intraocular disorders. I. A colocalisation study of the serum spreading factor, vitronectin, and fibronectin in traction membranes from patients with proliferative vitreoretinopathy

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

doi:10.1007/bf00224460

Cited by 23 publications

(10 citation statements)

References 31 publications

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“…A limited number of reports exist regarding details of cellular metabolism in macular pucker, RD and PVR. Also the glycoprotein vitronectin has been identified in epiretinal membranes 40 . This glycoprotein stabilizes PAI‐1 41 and mediates its binding to extracellular matrix 42 .…”

Section: Discussionmentioning

confidence: 99%

Components of the fibrinolytic system in the vitreous body in patients with vitreoretinal disorders

Ulrich

Spannagl

Gandorfer

2008

Clinical Exper Ophthalmology

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Purpose: To assess components of the fibrinolytic system in the vitreous humour and serum of patients with vitreoretinal disorders. Methods: Forty‐three samples of vitreous humour and plasma of 43 patients undergoing pars plana vitrectomy for macular hole, macular pucker, retinal detachment or proliferative vitreoretinopathy were evaluated for their content of plasminogen, a2‐antiplasmin, plasminogen‐activator‐inhibitor 1, plasmin‐a2‐antiplasmin‐complex, tissue plasminogen activator, total protein, albumin, d‐dimer. Patient groups were compared with each other using the U‐test (Mann and Whitney) for non‐parametric testing of two independent samples. Results: The groups of retinal detachment and proliferative vitreoretinopathy had elevated vitreal levels of plasminogen‐activator‐inhibitor 1 (352.5 and 370.7 ng/mL vs. 1.86 and 56.6 ng/mL, P = non‐significant), plasmin‐a2‐antiplasmin‐complex (2416.5 and 1836.2 µg/L vs. 124.2 and 133.4 µg/L, P < 0.001), albumin (0.08 and 0.15 g/dL vs. 0.03 and 0.07 g/dL, P < 0.05) and d‐dimer (4.76 and 1.64 µg/mL vs. 0.40 and 0.48 µg/mL, P = non‐significant) when compared with patients with macular hole and macular pucker. Conclusions: There are significant differences in the vitreal concentration of components of the fibrinolytic system in patients with vitreoretinal disorders. Breakdown of the blood–retinal barrier and complex disease‐specific mechanisms are thought to be responsible for an increase of components of the fibrinolytic system in the vitreous.

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Section: Discussionmentioning

confidence: 99%

Components of the fibrinolytic system in the vitreous body in patients with vitreoretinal disorders

Ulrich

Spannagl

Gandorfer

2008

Clinical Exper Ophthalmology

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“…Alteration of coagulation factors, especially increased levels of antithrombin III, have been reported 3839 We have previously reported the presence of vitronectin in epiretinal membranes40 and elevated plasma levels of this protein in diabetic patients 2241 stabilises plasminogen activator inhibitor-1 (PAI-1),42 and mediates PAI-1 binding to extracellular matrix 43…”

Section: Discussionmentioning

confidence: 99%

Plasminogen in proliferative vitreoretinal disorders

Esser

Heimann²,

Bartz‐Schmidt³

et al. 1997

British Journal of Ophthalmology

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Objective-Intravitreal fibrin formation is a frequent observation after vitrectomy performed for a variety of vitreoretinal disorders including proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), and endophthalmitis. Plasminogen activators (PA) have been used for the management of this postoperative complication. This approach requires the presence of plasminogen, the substrate for PA mediated fibrinolysis, in the vitreal cavity. Methods-Quantification of plasminogen in the vitreous of 60 patients with PVR, PDR, and macular pucker was performed by streptokinase mediated activation using a chromogenic substrate. The presence of immunoreactive plasminogen was confirmed by immunoblot analysis of vitreal proteins and immunocytochemistry of surgically removed epiretinal membranes. Results-Plasminogen levels were dramatically increased in the vitreous of PVR and PDR patients compared with macular pucker patients and normal controls. Staining for plasminogen in epiretinal membranes was confined to the extracellular matrix. Predominant staining of perivascular areas in PDR specimens indicated that breakdown of the bloodretinal barrier is an important source of intravitreal plasminogen in that condition. Conclusion-Plasminogen may play a role in traction membrane formation in PVR and PDR. Our biochemical analysis of presurgical vitreous indicates that there may be abundant substrate for PA mediated fibrinolysis in the vitreous cavity after vitrectomy. (Br J Ophthalmol 1997;81:590-594)

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“…Similarly, the levels of intravitreal fibronectin, an indicator of proliferative process activity [47], are higher in vitreous aspirates from patients with traumatic PVR, especially in relation to the total protein content of the vitreous samples [124]. Immunofluorescence labeling of periretinal membranes for the serum spreading factor, vitronectin, has produced a third piece of evidence for a different course in idiopathic and traumatic PVR [122]. None of these findings, however, proves a qualitative difference between traumatic and idiopathic PVR.…”

Section: Resultsmentioning

confidence: 88%

“…Progress in the insight into the pathogenesis of PVR will be made more rapidly by the analysis of human vitreous aspirates and periretinal membranes than by animal models of PVR. Recent ideas which have introduced new aspects of PVR involved TGF-~ [34,35], transferrin [125], and vitronectin [122]. None of these studies was based on an animal model.…”

Section: Resultsmentioning

confidence: 99%

“…The important role of fibronectin can be deduced from interactions with all six cellular elements involved in soft tissue repair (see above). It remains to be seen whether the presence of the serum spreading factor, vitronectin, in periretinal membranes [122] will be confirmed in future studies on would healing elsewhere in the body. Both fibronectin and vitronectin belong to a class of distict attachment proteins which exhibit a cell binding domain containing the amino acid sequence arg-gly-asp or, following the amino acid code, RGD [1,9,97].…”

Section: The Extracellular Matrixmentioning

confidence: 99%

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Proliferative vitreoretinopathy ? is it anything more than wound healing at the wrong place?

Weller¹,

Wiedemann²,

Heimann³

1990

Int Ophthalmol

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Proliferative vitreoretinopathy (PVR) is a reactive process of the ocular tissue after perforating trauma, retinal detachment, and surgical manipulations. Although several studies, most of them experimental, have focused on the detection of specific etiologic factors in the development of PVR, there is compelling evidence that PVR is nothing more than a physiologic tissue repair process with undesirable consequences for the retina. Important features of PVR involving the role of platelets, mononuclear phagocytes, and fibroblasts parallel the chain of events observed in tissue repair elsewhere in the body. Numerous experimental models for PVR, originally designed to find specific stimuli for the generation of intraocular traction membrane formation, have shown that the process of PVR is the common pathway of the eye's reaction to vitreoretinal trauma of any kind. Accordingly, vitreoretinal surgeons could learn a lot from the work of other disciplines, e.g. surgery and dermatology, on wound healing, and the factors known to modify wound healing elsewhere in the body should be taken into consideration. The well-established impairment of tissue repair processes caused by medical treatment with corticosteroids and cytotoxic agents suggests a combined medical approach to PVR as an adjunct to surgical treatment, using refined methods of application and dosage. Steroids and cytotoxic drugs will influence the course of PVR by suppressing macrophage recruitment and the initial inflammatory reaction as well as the proliferative phase of wound healing with traction retinal detachment, respectively.

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Vitronectin and proliferative intraocular disorders. I. A colocalisation study of the serum spreading factor, vitronectin, and fibronectin in traction membranes from patients with proliferative vitreoretinopathy

Cited by 23 publications

References 31 publications

Components of the fibrinolytic system in the vitreous body in patients with vitreoretinal disorders

Components of the fibrinolytic system in the vitreous body in patients with vitreoretinal disorders

Plasminogen in proliferative vitreoretinal disorders

Proliferative vitreoretinopathy ? is it anything more than wound healing at the wrong place?

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