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PubMedDate not supplied

Growth factors in retinal diseases: proliferative vitreoretinopathy, proliferative diabetic retinopathy, and retinal degeneration.

The goal of this review is to present the current knowledge on specific growth factor involvement in posterior segment eye disease. Growth factors can be defined as multifunctional signals which modify cell growth or proliferation, alone or in concert, by binding to specific cell surface receptors. Their biological effects on cells include cell adhesion, migration, survival, differentiation, extracellular matrix secretion, protease and protease inhibitor release, production of other growth activities, and angiogenesis. Growth factors couple the cell to the microenvironment. As some growth factors are soluble mediators of wound repair and angiogenesis, it seems possible that proliferative vitreoretinopathy and proliferative diabetic retinopathy are caused or aggravated by these factors. Other factors act as survival factors and can possibly prevent retinal degeneration. The multifunctional nature of growth factors makes it probable that practical uses will be found for these agents in the future.

Diabetic Retinopathy↗

PubMed1998

Induction of arachidonic acid metabolite release by human fibroblasts in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy is a severe ocular disorder characterized by unwanted proliferation of cells and excessive production of fibrous tissue, which leads to the formation of cellular membranes on the surface of the retina and in the vitreous. Proliferative vitreoretinopathy is the most common cause of failure in retinal reattachment surgery, approximately occurring in one out of ten operated eyes. Proliferation of retinal pigment epithelial cells and fibroblasts is a cornerstone in the pathogenesis of proliferative vitreoretinopathy. An in vitro-proliferation assay showed previously that intraocular fluid from patients with proliferative vitreoretinopathy is potently effective in stimulating proliferation of human fibroblasts. Here we show that exposure of human fibroblasts to vitreous fluids from patients with proliferative vitreoretinopathy causes a rapid and sustained increase in arachidonic acid metabolite release as measured by competitive enzyme-immunoassay. The findings implicate prostaglandin E2 as a contributor to enhanced intraocular fibrosis in proliferative vitreoretinopathy. As prostaglandin E2 is a mediator of continuous aqueous-blood retinal barrier breakdown in this severe disease, cycclooxygenase inhibitors such as acetylsalicylic acid, which was successfully used in this study for blocking the effect of intraocular fluid, may be useful agents in targeting the progression of intraocular fibrosis.

Adult↗

PubMedDate not supplied

Elevated levels of substance P in intraocular fluid in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy is the most common reason for failure in retinal reattachment surgery. Since both substance P (SP) and SP receptors were found to be present in the human eye, and as pharmacological studies suggest an importance of SP for ocular functions, we investigated intraocular fluids for the presence of SP in eyes elected for cataract surgery, retinal detachment surgery and retina surgery for severe proliferative vitreoretinopathy (PVR) as well as in eyes with proliferative diabetic retinopathy (PDR). High performance liquid chromatography and radioimmunoassay (RIA) for SP immunoreactivities were performed. The SP mean concentration in intraocular fluid (IOF) of patients for cataract surgery (CS) was 2.2 fmol/ml, for retinal detachment (RD) was 2.7 fmol/ml and for PDR was 1.9 fmol/ml; significantly higher levels (mean concentration of 26.9 fmol/ml) were measured in eyes with PVR. HPLC analysis revealed two immunoreactive peaks coeluting with synthetic SP and SP-sulfoxide, indicating that RIA values represent authentic SP. We conclude that SP may play an important role in PVR. Since SP antagonists are known to inhibit a variety of SP effects in the eye, there might be a useful tool to reveal the importance of SP in this disease and, in this instance, a new possible treatment.

Adult↗

PubMed2004

[Pharmacological adjuvants for surgical treatment of proliferative vitreoretinopathy].

Proliferative vitreoretinopathy (PVR) is the major cause of retinal detachment surgery failure. Many adjuvants were studied in vitro and on animals, some were studied on humans. Daunomycin seems to reduce PVR recidivism. 5-FU and steroids are nontoxic but their efficacy is not clear. Heparin reduced postoperative inflammation and seems to reduce PVR recidivism when associated with 5-FU. Associating heparin and steroids seems to reduce PVR in some groups of patients (aphakic, anterior PVR). Colchicine and retinoic acid per os are ineffective, silicone oil is effective as an internal tamponade but not as an adjuvant of PVR. Currently, no molecule has proven efficacy as an adjunctive treatment of PVR.

Chemotherapy, Adjuvant↗

PubMed1998

Risk factors for proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) is one of the major causes of failure in retinal detachment surgery. To prevent PVR, it is necessary to determine factors predisposing its development. In primary PVR, large retinal tears, long duration of retinal detachment, vitreous hemorrhages, aphakia and choroidal detachment were demonstrated as clinical risk factors for PVR. In postoperative PVR, it was revealed that large breaks, pre- and postoperative choroidal detachment, minor intra- or postoperative hemorrhages, signs of uveitis, extensive retinal detachment, vitrectomy, cryopexy, air injection and preoperative PVR were risk factors for PVR by multivariate analysis. Almost all risk factors for PVR are associated with intravitreal dispersion of retinal pigment epithelial (RPE) cells or breakdown of the blood-ocular barrier which are prerequisite to development of PVR.

Animals↗

PubMed1995

Epidermal dipeptide: a new regulatory factor in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) is the most severe complication of retinal detachment surgery, occurring approximately in one out of ten operated eyes. The proliferation of retinal pigment epithelial (RPE) cells and fibroblasts is a cornerstone in the pathogenesis of PVR. Since inhibitory peptides may take a part in the feedback mechanism underlying this proliferation, we assessed the effect of synthesized epidermal dipeptide, pyroglu-glyOH (EDP), on the proliferation of RPE cells and fibroblasts in vitro. The maximum inhibitory effect of EDP on the RPE cells was reached at concentrations ranging from 1.07*10(-13) to 1.07*10(-15) M. Its inhibitory effect on fibroblasts followed a similar pattern at all concentrations applied, 1.07*10(-6) to 1.07*10(-15) M. These results enhance the possibility that PVR may be due to an imbalance of inhibition/disinhibition mechanism under participation of several regulatory molecules like EDP. EDP might have the potential for reducing the risk of PVR.

Animals↗

PubMed1986

Proliferative vitreoretinopathy.

Proliferative vitreoretinopathy is the recently adopted term for a complicating condition which occasionally follows retinal detachment. The major processes involved are cellular proliferation and membrane formation. These developments greatly reduce the surgical success rate. A case of proliferative vitreoretinopathy is presented here; we briefly review the mechanism of development of this condition, as well as current treatment concepts.

Adult↗

PubMed1991

Immunocytology of cellular components in vitreous and subretinal fluid from patients with proliferative vitreoretinopathy.

Proliferative vitreoretinopathy accounts for most of failures in retinal detachment surgery. It results from the formation of membranes spreading onto inner and outer surfaces of the detached retina and within the vitreous body, but the nature of the growing cells and the mechanisms of proliferation remain speculative. A cytological study was thus undertaken on 35 specimens of vitreous and subretinal fluid obtained surgically in patients with proliferative vitreoretinopathy. Various types of cells were identified: typical pigment epithelial cells, lightly pigmented and large totally unpigmented macrophage-resembling cells, smaller unpigmented cells and lymphocytes. Immunocytological procedures with 10 different monoclonal antibodies directed against different markers of epithelial and immunocompetent cells showed the epithelial nonmacrophagic origin of the intravitreal and subretinal cells, as most of these cells were positive for cytokeratin but remained negative for macrophage markers. Examination of intravitreal pigment granules, using autofluorescence analysis by epi-illumination and toluidine blue staining, showed two distinct populations of pigmented cells, one containing melanin and the other lipofuscin, suggesting that pigmented cells could originate from the retinal and ciliary pigment epithelia. As concerns lymphocyte identification, only B cells were seen, whereas no T lymphocyte could be found. Fibronectin was found on a minority of cells in 4 vitreous specimens, but cells positive for glial fibrillary acidic protein could not be seen. These results confirm the involvement of pigment epithelial cells and the strong morphological changes they undergo during the course of proliferative vitoretinopathy, but the mechanisms of proliferative phenomena after retinal detachment remain to be determined.

Adolescent↗

PubMed1992

[Pathogenesis of traumatic proliferative vitreoretinopathy].

Proliferative vitreoretinopathy is the main cause of loss of vision following posterior penetrating eye injury. Clinically, it can range from macular epiretinal membrane to total retinal detachment and phthisis bulbi. To gain more knowledge of its pathogenesis, the author performed morphologic studies using a primate model and also studied the distribution of fibronectin in 13 enucleated patient eyes using immunofluorescent histochemical techniques. Results indicate this disease process represents an overstimulated response to retinal injury. Posterior vitreous detachment at the level of internal limiting membrane appears to be a predisposing factor. During the active phase of the disease process, there is selective increase of fibronectin in the choroid. This increase is not merely due to the passive leakage of plasma caused by the injury, but the choroid itself produces cellular fibronectin. Fibronectin is known to enhance wound healing and may be an important factor in the pathogenesis of proliferative vitreoretinopathy.

Animals↗

PubMed1998

C-C chemokines in the vitreous of patients with proliferative vitreoretinopathy and proliferative diabetic retinopathy.

PURPOSE: To investigate the presence of three C-C chemokines (monocyte chemotactic protein-1 [MCP-1], macrophage inflammatory protein-1alpha [MIP-1alpha], and MIP-1beta) in vitreous samples from eyes with proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), or retinal detachment (RD). SUBJECTS AND METHODS: Vitreous samples were obtained and assayed by solid phase enzyme-linked immunosorbent assay for the chemokines MCP-1, MIP-1alpha, and MIP-1beta in a prospective study of 43 consecutive patients. Eighteen samples from cadaveric control eyes were also assayed. RESULTS: Monocyte chemotactic protein-1 was detected in all samples. The vitreous of eyes with vitreoretinal disorders showed significantly higher levels than the vitreous of cadaveric control eyes (P < or = 0.05). Median level (5th-95th percentile) in the PVR cases (n = 20) was 890.18 pg/mL (286.04-1806.20); in RD (n = 8), 296.69 pg/mL (171.44-1310.02); and in PDR (n = 15), 434.60 pg/mL (124.56-1092.94). In the cadaveric control eyes (n = 18), median level was 83.97 pg/mL (26.09-208.38). Macrophage inflammatory protein-1alpha and MIP-1beta were not detected in any samples. CONCLUSION: Monocyte chemotactic protein-1 might be involved in the recruitment of macrophages and monocytes into the vitreous of eyes with proliferative vitreoretinal disorders.

Biomarkers↗

PubMed1988

Immunochemical studies of epiretinal membranes using APAAP complexes: evidence for macrophage involvement in traumatic proliferative vitreoretinopathy.

Proliferative vitreoretinopathy is characterized by cellular proliferations in the periretinal space resulting in traction retinal detachment. Numerous cellular elements and connective tissue components have been identified by morphologic criteria as well as immunochemical techniques. In this study, we used the recently introduced APAAP (alkaline phosphatase - anti-alkaline phosphatase) immunostaining procedure to identify macrophages, T-lymphocytes, the structural proteins fibronectin, vimentin, and cytokeratin, and a proliferating cell antigen, in eleven human epiretinal membranes obtained during vitreoretinal surgery. Our results confirm that the pathologic processes in PVR are not immunologically mediated, but reveal the features of physiologic wound healing and scar formation. Posttraumatic PVR seems to be characterized by a severe initial inflammatory reaction as evidenced by the presence of numerous macrophages, whereas idiopathic PVR, as a complication of retinal detachment, may be caused by different mechanisms in the early pathogenesis.

Alkaline Phosphatase↗

PubMed1990

Autoimmune responsiveness to retinal IRBP, S-antigen and opsin in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) was induced in rabbits by intravitreal injection of homologous fibroblasts. During the 8 weeks after injection the immune responsiveness to three purified retinal autoantigens was studied. From 2 weeks after injection, animals that developed serious forms of PVR exhibited definite mitotic responses of their lymphocytes to stimulation by the retinal antigens. These responses could consistently be demonstrated for S-antigen and interphotoreceptor retinoid-binding protein (IRBP) during the subsequent period of examination. Marked responses were also noted to opsin, however, their occurrence was more variable. In mild forms of PVR or in controls the responses were weak or absent. This showed that the elevated cellular reactivities were induced by the development of PVR and not by some other experimental factor. Humoral immune responses to the three antigens were absent (as assayed by ELISA). The control groups did not exhibit any elevated immune responsiveness. There appears to be accumulating evidence that inflammation may play a role in the development of PVR. The present results indicate that cellular autoimmune responses to photoreceptor antigens are a secondary phenomenon in PVR, nevertheless, they may be an important factor in the subsequent development of severe PVR. This autosensitization may consequently be taken into consideration in the treatment of complicated human PVR.

Animals↗

PubMed1991

Class II histocompatibility antigen expression by cellular components of vitreous and subretinal fluid in proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) is the major cause of failure in retinal detachment surgery. It is characterized by the formation of membranes extending along both surfaces of the detached retina and within the vitreous, but the nature of the growing cells has not yet been determined. Using cytologic and immunocytologic procedures with 13 different monoclonal antibodies directed against Class II histocompatibility antigens and various markers of epithelial and immunocompetent cells, 30 specimens were studied of vitreous or subretinal fluid removed from patients with PVR. Five main types of cells could be identified: heavily pigmented cells, poorly pigmented ones, large totally unpigmented macrophage-resembling ones, smaller unpigmented cells, and lymphocytes. Analysis of intravitreal pigment granules, using autofluorescence by epiillumination and cytologic procedures, showed two different populations of pigmented cells: one with autofluorescent lipofuscin granules and the other with exclusively melanin pigment. Immunostaining procedures confirmed the epithelial nonmacrophage lineage of the intravitreal and subretinal cells because most of these cells were positive for cytokeratin but negative for macrophage markers. In addition, 40-100% of these epithelial-derived cells strongly expressed Class II histocompatibility antigens HLA-DR and -DQ. Lymphocytes were found in 13 specimens; B-cells were seen, but no T-lymphocytes could be identified. These results confirm the involvement of retinal pigment epithelial cells and the strong morphologic changes they undergo during the course of PVR. Moreover, the expression of Class II histocompatibility antigens by the growing cells may be related to inflammatory phenomena, but their eventual role in the development and the extension of periretinal proliferation has not been determined.

Adolescent↗

PubMed1985

Taxol for the treatment of proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) results in retinal detachment and visual impairment due to fibroblastic proliferation in the vitreous and subsequent cellular contraction. The authors have used an in vitro model for PVR to evaluate the action of the antineoplastic drug, taxol, on chorioretinal fibroblast proliferation and contractility. Dose response curves obtained show taxol to be a potent inhibitor of both cellular events. Fifty percent inhibition of contraction and proliferation occurred at 2 X 10(-8)M and 3 X 10(-9)M, respectively. On the basis of this pharmacodynamic data, three dosage regimes were chosen to evaluate possible prevention of PVR in an animal model based on the intravitreal injection of cultured fibroblasts. These animals trials show that a single intravitreal dose of either 35 micrograms or 0.5 microgram taxol significantly reduces incidence and extent of PVR. The average grade of vitreoretinal traction at 28 days for 35 micrograms taxol and 250,000 cells was 0.4 (control 1.8); for 35 micrograms taxol and 700,000 cells, 1.0 (control 2.2); and for 0.5 microgram taxol and 250,000 cells, 1.0 (control 2.3). Delayed optic nerve damage was noted with the highest dose used, but a good therapeutic margin may exist. Long-term clinical histopathologic and electrophysiologic studies will be required. The authors conclude from these preliminary studies that taxol holds definite promise for the relief of traction retinal detachment and PVR.

Alkaloids↗

PubMedDate not supplied

Interleukin (IL)-6, interleukin (IL)-8 levels and cellular composition of the vitreous humor in proliferative diabetic retinopathy, proliferative vitreoretinopathy, and traumatic proliferative vitreoretinopathy.

PURPOSE: To investigate the interleukin (IL)-6 levels, IL-8 levels, and cellular composition of the vitreous humor in patients with proliferative diabetic retinopathy (PDR), proliferative vitreoretinopathy (PVR), and traumatic PVR. METHODS: Vitreous samples from 14 patients with PDR, 10 patients with PVR, and 10 patients with traumatic PVR were analyzed. Fifteen cadaver eyes were used as controls. Cytokine levels were measured by ELISA. RESULTS: Elevated IL-6 levels were detected in the vitreous of 12 (85.7%) of the PDR patients, eight (80%) of the PVR patients, and all (100%) of the traumatic PVR patients. None of the control IL-6 results were elevated. Vitreous IL-8 levels were elevated in 12 (85.7%) of the PDR patients, six (60%) of the PVR patients, all (100%) of the traumatic PVR patients, and one (6.7%) of the control eyes. Cytological examination of the vitreous specimens revealed a predominance of macrophages (50%) in the PDR samples and a predominance of retinal pigment epithelial (RPE) cells (60%) in the PVR samples. In contrast, neutrophils predominated (88%) in the traumatic PVR samples. CONCLUSION: The findings suggest that IL-6 and IL-8 may be involved in the pathogenesis of PDR, PVR, and traumatic PVR. High proportions of RPE cells and macrophages are associated with elevated IL-6 and IL-8 levels in the vitreous of PDR and PVR patients; however, the fact that these cells are not predominant in traumatic PVR suggests that different immune response mechanisms may be active in the pathogenesis of these disorders.

Adolescent↗

PubMed1993

Origin of fibronectin in epiretinal membranes of proliferative vitreoretinopathy and proliferative diabetic retinopathy.

Fibronectins, high molecular multifunctional glycoproteins of the extracellular matrix and plasma, have been a popular area of research in the pathogenesis of proliferative disorders of the retina. Several immunohistochemical studies have revealed that fibronectin is a major constituent of epiretinal membranes and that the cell types involved in proliferative intraocular disorders may synthesise it. However, owing to the fact that plasma and cellular fibronectin are similar in their overall structure, the origin of fibronectin in epiretinal membranes has not yet been clearly defined. In this study, we used two monoclonal antibodies: FN-3, which recognises an extra domain present in the cellular but not plasma form of fibronectin; and FN-4, which reacts with an antigenic site on both plasma and cellular fibronectin. In 37 epiretinal membranes obtained from eyes with proliferative vitreoretinopathy and proliferative diabetic retinopathy, we demonstrated the presence of cellular fibronectin, thus indicating local production. The significantly stronger and positive immunostain with FN-4 in the same specimens suggests the colocalisation of plasma fibronectin, that may be derived from the breakdown of the blood-retinal barrier and trapped in membranes during their formation. In pathological vitreous we demonstrated both types of fibronectin by western blot analysis.

Blotting, Western↗

PubMedDate not supplied

Interleukin-8, nitric oxide and glutathione status in proliferative vitreoretinopathy and proliferative diabetic retinopathy.

PURPOSE: To evaluate interleukin-8 (IL-8), nitric oxide (NO) and glutathione (GSH) profiles in vitreous humor and blood samples in patients with proliferative diabetic retinopathy (PDR) and in patients with proliferative vitreoretinopathy (PVR) and to compare the levels with those of controls. PATIENTS AND METHODS: NO concentrations were determined by using the Greiss reaction in plasma and vitreous humor samples. GSH levels were determined in both blood and vitreous humor samples, using DTNB, a disulfide chromogen. Vitreous IL-8 were assayed by ELISA. Twenty-three patients with PDR, 18 patients with PVR and 21 cadavers as the control group were included in the study. RESULTS: Plasma and vitreous NO levels were found to be 25.6 +/- 2.1 and 36.9 +/- 3.0 micromol/l in patients with PDR, 27.0 +/- 4.7 and 34.3 +/- 2.9 micromol/l in patients with PVR and 17.4 +/- 2.7 and 15.9 +/- 1.4 micromol/l in controls, respectively. Vitreous humor and plasma NO levels did not show any statistically significant difference between PDR and PVR groups. However, the values for vitreous in both groups were significantly higher than those of controls (p < 0.0001). Although IL-8 levels in vitreous samples of patients with PDR were not significantly different (79.6 +/- 9.7 pg/ml) from those of patients with PVR (42.2 +/- 7.3 pg/ml) (p = 0.06), the levels in both groups were significantly higher than those of controls (19.0 +/- 3.9 pg/ml) (p < 0.0001 and p < 0.05, respectively). Blood and vitreous GSH levels were found to be 5.3 +/- 0.4 micromol/g. Hb and 0.58 +/- 0.16 micromol/l in patients with PDR and 8.4 +/- 0.5 micromol/g. Hb and 15.7 +/- 2.2 micromol/l in patients with PVR and 12.0 +/- 1.1 micromol/g. Hb and 0.26 +/- 0.03 mmol/l in controls, respectively. Vitreous and blood GSH levels were significantly lower in patients with PDR compared to those with PVR (p < 0.0001 for both). CONCLUSION: Elevated levels of vitreous and plasma NO and vitreous IL-8 in PDR and PVR implicate a role for these parameters in the proliferation in these ocular disorders. GSH concentrations both in vitreous and blood samples of the PVR and PDR patients were much less than those observed in the control group. Lower GSH concentrations detected in PDR in comparison with those in PVR in vitreous humor and to a lesser degree in blood may play an important role in pathogenesis of new retinal vessel formation in patients with PDR. This also suggests that oxidative stress may be involved in the pathogenesis of PVR and particularly that of PDR.

Adult↗

PubMed1999

Soluble cellular adhesion molecules in proliferative vitreoretinopathy and proliferative diabetic retinopathy.

PURPOSE: To measure vitreous levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cellular adhesion molecule-1 (sVCAM-1) in the eyes of patients with retinal detachment (RD) due to proliferative diabetic retinopathy (PDR) or proliferative vitreoretinopathy (PVR) and to determine whether the levels of these mediators correlated with clinical parameters of disease. METHODS: Undiluted vitreous specimens were collected from 50 eyes of 48 patients undergoing vitrectomy for traction RD due to PDR (21 specimens) and recurrent RD due to PVR (19 specimens). Control vitreous specimens were obtained from patients undergoing macular hole repair (10 specimens). The levels of sICAM-1 and sVCAM-1 were measured in each sample by specific enzyme-linked immunoadsorbent assays. RESULTS: Vitreous levels of sICAM-1 were significantly increased in vitreous specimens from both PVR (median +/- SD; 12.0 +/- 76.3 ng/ml; P < 0.01) and PDR (8.4 +/- 24.0 ng/ml; P < 0.01) when compared to vitreous from eyes with macular holes (0. 3 +/- 4.2 ng/ml). Vitreous levels of sVCAM-1 were significantly increased in both PVR (36.5 +/- 255.2 ng/ml; P < 0.001) and PDR (26. 2 +/- 93.5 ng/ml; P < 0.01) when compared to control vitreous (17.7 +/- 7.8 ng/ml). The vitreous levels of sICAM-1 were higher in cases of PDR which developed recurrent proliferative disease (P < 0.01) and recurrent RD (P = 0.01), whereas the levels of sICAM-1 in PVR and sVCAM-1 in PDR and PVR did not significantly correlate with these clinical parameters. CONCLUSIONS: Soluble forms of ICAM-1 and VCAM-1 are increased in the vitreous cavity of patients with RD due to PDR or PVR, reflecting the inflammatory nature of these conditions and suggesting a possible role for these mediators in the pathogenesis of proliferative retinal disease. The vitreous levels of these sCAMs at the time of surgery may serve as a marker of inflammation, but their specific levels do not predict the likelihood of recurrent proliferation or surgical anatomic success in most cases of PVR and PDR.

Adult↗