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Biomedical subjects

S J Ryan

Publications and source records attributed to S J Ryan.

At least 127 records · Page 7Linked to original sources
PubMed1989

Vitreous modulation of migration and proliferation of retinal pigment epithelial cells in vitro.

Retinal pigment epithelial (RPE) cell migration and proliferation are believed to play a role in the pathogenesis of proliferative vitreoretinopathy (PVR). Since PVR develops in situations where vitreous contacts the RPE, we sought to determine whether human vitreous contains factors that stimulate proliferation and migration of RPE cells. We found that postmortem human vitreous stimulates migration but not proliferation of human RPE cells under serum-free conditions in vitro. Stimulation of proliferation of RPE cells and fibroblasts was observed, however, following admixture of albumin with the vitreous. These findings suggest that vitreous contributes modulators that stimulate some functions of RPE cells that are believed to play a role in the pathogenesis of PVR.

Cell Division↗
PubMed1989

Subretinal choroidal neovascularization as a response to penetrating retinal injury in the pigmented rabbit.

Subretinal choroidal neovascularization has been identified in the pigmented rabbit in association with penetrating retinal injury. In this study, the subretinal new vessels were not contained within the fibrous scar, but were located posterior to it and impinged on the visual streak. Histology revealed subretinal neovascularization in the region of transition from normal to atrophic retina. These new vessels originated from the choroidal vessels and extended through a spontaneous break in Bruch's membrane into the retinal pigment epithelium. There was degeneration of the photoreceptors and hyperplasia of the retinal pigment epithelium in the region of neovascularization. The subretinal new vessels identified in the pigmented rabbit have many of the morphological features seen in the human clinical condition, and therefore this animal model may be useful in studying human choroidal neovascularization.

Animals↗
PubMed1988

Cellular proliferation induced by subretinal injection of vitreous in the rabbit.

A new experimental model of subretinal cellular proliferation, based on injection of autologous vitreous into the subretinal space of rabbits, was studied by light and electron microscopy. As early as five days after injection, proliferation of retinal pigment epithelial (RPE) and retinal glial cells was observed in the subretinal space. These morphologically distinct proliferating cells were sometimes joined by junctional complexes. Morphologically, the proliferating RPE cells resembled either RPE cells or fibroblasts. Some proliferating RPE cells also retained their epithelial characteristics (ie, basement membranes and cell junctions), while others were partially dedifferentiated and showed some embryonic features. New formation of melanin could be identified within the proliferated RPE cells, which could account, in part, for the hyperpigmentation at the site of the bleb caused by the injection of vitreous. The results demonstrated that injection of autologous vitreous into the subretinal space can lead to subretinal proliferation of retinal glial and RPE cells in the rabbit.

Animals↗
PubMed1988

Glial epiretinal membranes and contraction. Immunohistochemical and morphological studies.

It has been suggested that glial cells do not contribute substantially to the contractile forces generated by epiretinal membranes. We have established a rabbit model in which epiretinal membranes form on the inferior peripheral retina after the injection of activated macrophages into the vitreous. By two months, the membranes were extensive but without evidence of traction. At four months, however, full-thickness retinal folds were present beneath the thick epiretinal membrane. A homogeneous glial cell composition was suggested by light microscopic examination of serial sections through several membranes. Immunohistochemical staining with anti-glial fibrillary acidic protein and antivimentin and immunoelectron microscopy confirmed that these thick epiretinal membranes were composed entirely of glial cells, which may cause mild traction on the retina; this traction is associated with cell alignment and the tissue bridges connecting the membrane and the retina. The fusiform densities and indented nuclei suggested that the glial cells within the membrane may possess some characteristics of myofibroblasts.

Animals↗
PubMed1988

Human retinal pigment epithelial cell cultures: phenotypic modulation by vitreous and macrophages.

In proliferative vitreoretinopathy (PVR), retinal pigment epithelial (RPE) cells migrate into the vitreous, where they may acquire a fibroblast-like morphology. Such cells may eventually form contractile periretinal membranes, resulting in traction retinal detachment. Among the environmental influences that could cause this change in RPE phenotype, exposure to vitreous and to macrophages is most obvious, as macrophages are invariably found in epiretinal membranes and precede membrane formation in experimental traction retinal detachment. We initiated studies to define modulation of cultured RPE cell morphology by exposure to vitreous or to macrophage-conditioned media. Vitreous, serum, and albumin alone had no effect on the epithelial appearance of RPE cells in vitro. However, macrophage-conditioned media and vitreous-serum or vitreous-albumin mixtures induced a reversible fibroblast-like appearance in these cells. These findings show that macrophages produce a morphoplastic substance for RPE cells, and suggest that vitreous also contains a factor(s) that affects RPE cell shape, and that requires mediation by serum components.

Actins↗
PubMed1988

Breakdown of Bruch's membrane after subretinal injection of vitreous. Role of cellular processes.

It was recently shown that the injection of autologous vitreous beneath the retina of rabbits leads to retinal degeneration, subretinal cellular proliferation and neovascularization. The current study, using electron microscopy, was designed to determine the cellular processes involved in the breakdown of Bruch's membrane in this model. Bruch's membrane was not mechanically damaged by the injection and appeared intact for the first 1 to 2 days after injection. Subsequently, numerous breaks in Bruch's membrane were found associated with invasion of macrophages and fibroblasts; in addition, budding and penetration of retinal pigment epithelial (RPE) and choroidal endothelial cells into Bruch's membrane were noted. Although it was not proven that these cells, per se, were responsible for the breaks, that these cells actively penetrate Bruch's membrane is a reasonable hypothesis.

Animals↗
PubMed1988

Experimental changes resembling the pathology of drusen in Bruch's membrane in the rabbit.

Drusen-like changes in Bruch's membrane following subretinal injection of vitreous in the rabbit were studied by electron microscopy. A sequence of changes is seen that closely panellels those observed during drusen formation in primates. The initial event is the budding of retinal pigment epithelial (RPE) cells into Bruch's membrane; the buds, which contain cytoplasm and plasma membrane, are connected to the cytoplasm of the parent RPE cell. Most buds are surrounded by basement membrane, but some penetrate RPE basement membrane into Bruch's membrane. Later, RPE buds completely separate from the parent RPE cell and show degeneration and disintegration. Finally, drusen-like material, including vesicular, granular, tubular and linear structures, is dispersed from the bud remnant into Bruch's membrane. The study described herein thus supports the hypothesis that drusen are the result of budding from the RPE.

Animals↗
PubMed1988

Liquefaction of rabbit vitreous by ferrous ions.

Intravitreal injection of 0.7 mumol of ferrous chloride in 0.1 ml into the rabbit eye resulted in liquefaction of the vitreous gel and condensation of vitreous collagen fibrils within two weeks; injection of 0.1 mumol did not cause any obvious vitreous degeneration, although retina damage was noted in the posterior pole. Macrophages migrated at the vitreoretinal interface and local posterior vitreous separation was observed after the injection of ferrous solution. This suggests that the least amount of ferrous ions necessary to cause liquefaction of the rabbit vitreous is in the range of 16.8 to 39.2 micrograms of elemental iron, a concentration of 0.3 to 0.7 mM in the vitreous. Since 0.1 ml of blood contains approximately 50 micrograms of iron, it is possible, at least theoretically, that the iron released by hemoglobin following vitreous hemorrhage could induce liquefaction of the vitreous.

Animals↗
PubMed1987

Intraoperative argon endophotocoagulation for recurrent vitreous hemorrhage after vitrectomy for diabetic retinopathy.

We reviewed the medical records of 103 consecutive cases of vitrectomy performed for complications of diabetic retinopathy to determine if the introduction of argon laser endophotocoagulation had reduced the incidence of recurrent vitreous hemorrhage. Twenty-six eyes (48%) treated with endophotocoagulation and 35 (71%) eyes not receiving laser treatment had a recurrent hemorrhage. Follow-up was shorter for the eyes treated with endophotocoagulation, but a log-rank analysis to allow for this variable confirmed the benefit of laser photocoagulation (P less than .05). The proportion of eyes requiring surgical removal of the hemorrhage was also significantly lower in the group receiving endophotocoagulation (P less than .05). The beneficial effect of intraoperative laser treatment was independent of the amount of preoperative laser treatment, aphakia, and indications for the original vitrectomy surgery.

Argon↗
PubMed1987

Posterior vitreous separation and retinal detachment induced by macrophages.

Macrophages, which migrate into the vitreous in conditions such as vitreous hemorrhage and penetrating ocular injury, may contribute to the development of intravitreous cellular proliferation and posterior vitreous separation. To investigate this possibility, activated macrophages were harvested from the peritoneal cavity and injected into the vitreous of rabbits. As early as 8 days after macrophage injection, posterior vitreous separation and glial epiretinal membrane formation began to occur. Two weeks after injection, vitreous strands that approached the optic disc and medullary rays were evident; fibroblasts proliferated over the disc or rays and induced retinal detachment. These findings support the hypothesis that macrophages in the vitreous may, in part, mediate cellular proliferation and posterior vitreous separation.

Animals↗
PubMed1987

Vitreoretinal junction in infectious endophthalmitis in a primate eye.

A primate eye affected by postoperative infectious endophthalmitis was studied early in the course of the disease. Retinal perivasculitis, vitreoretinal adhesions along the inflamed vessels, and traction of the partially separated posterior vitreous on the retina at the adhesion sites were observed. It is suggested that such vitreoretinal junction pathology may be responsible for the development of retinal detachment in infectious endophthalmitis.

Animals↗
PubMed1987

Morphologic observations on experimental subretinal neovascularization in the monkey.

Subretinal neovascularization is a poorly understood and potentially disastrous feature of many eye diseases. We used light and electron microscopy to study the sequence of events that lead to the formation of new vessels after laser photocoagulation of the retina and choroid of primates. In this animal model there is a rapid development of new blood vessels; one day after photocoagulation, endothelial cell degeneration and thrombus formation were observed in the capillaries, venules and arterioles of the choroid around the center of the lesion. Re-endothelialization began in some thrombosed choroidal vessels, with migration of the activated endothelial cells within the old basement membrane. Two days after photocoagulation, re-endothelialization was observed in almost all thrombosed choroidal vessels, and the initial stage of the endothelial cell budding was observed in the pre-existing choroidal vessels; this was especially prominent in venules with pericytes. Three days after photocoagulation, not only the endothelial cells in pre-existing vessels but also those in re-endothelialized vessels showed budding and lumen formation. The lumen of vessels was formed by the budding of adjacent endothelial cells that were coupled by transient intercellular junctions. Mitotic figures were frequently found in the endothelial cells distal to the growing tip. Five to eight days after photocoagulation, many new vessels extended into the subretinal space.

Animals↗
PubMed1987

Immunofluorescent studies of fibronectin and laminin in the human eye.

The topographic distribution of fibronectin and laminin in young and old human eyes was determined by indirect immunofluorescent techniques. These two glycoproteins may play a role in the attachment of the vitreous to the internal limiting membrane (ILM) and the internal limiting membrane to the Mueller cell processes. A double-laminated pattern of fluorescence for both glycoproteins was frequently found at the ILM of the posterior retina of aged eyes. This pattern of fluorescence, which was rarely seen in young eyes, may represent senescent changes in the ILM which could predispose the eye to posterior vitreous detachment.

Adolescent↗
PubMed1987

Alterations in the distribution of fibronectin and laminin in the diabetic human eye.

The distribution of fibronectin and laminin in diabetic human eyes was determined by indirect immunofluorescent techniques. The intense fluorescence suggests increased amounts of fibronectin and laminin in the diabetic internal limiting membrane (ILM). A double laminated pattern of fluorescence for both glycoproteins suggests structural abnormalities of the ILM of the posterior retina. Preretinal and subretinal proliferative tissues fluoresced strongly and diffusely with antifibronectin. This study indicates that in diabetic patients, the ILM, especially in the posterior retina, is biochemically and morphologically abnormal.

Aged↗
PubMed1986

Experimental epiretinal proliferation induced by intravitreal red blood cells.

We describe a reproducible animal model of epiretinal proliferation, based on intravitreal injection of red blood cells, that closely simulates the more benign proliferative extraretinopathies. Using light microscopy and scanning and transmission electron microscopy, we monitored the development and behavior of the experimental epiretinal membranes. We found breaks in the integrity of the retinal surface through which glial cells migrated onto the retina, proliferated into thick epiretinal tissue, and contracted to cause retinal pucker. All these steps were associated with the chronic inflammatory response to the long-lasting presence of red blood cells in the vitreous. Thus, the development of epiretinal membranes requires continuous intraocular stimulation in addition to a break in retinal integrity.

Animals↗
PubMed1986

Formation of drusen in the human eye.

Light and electron microscopy of drusen formation in the human eye showed yellow-white spots in the fundus with two morphologic patterns: that of typical drusen and a nodular accumulation of cellular components beneath the retinal pigment epithelial cells. By electron microscopy, the progression of drusen formation could be classified into four stages. Stage I showed budding or evagination of retinal pigment epithelial cells into the subpigment epithelial space. This evaginated portion was connected to the retinal pigment epithelial cell cytoplasm and was surrounded by its basement membrane. In Stage II the evaginated portion of the cell was completely separate from the cytoplasm of its parent retinal pigment epithelial cell. In Stage III, the evaginated portion showed degeneration and disintegration. Finally, in Stage IV, an accumulation of vesicular, granular, tubular, and linear material was seen free within the nodular space beneath the retinal pigment epithelial cell.

Aged↗
PubMed1986

Retinal wound healing. Cellular activity at the vitreoretinal interface.

Cellular activity at the vitreoretinal interface after full-thickness retinal wounds was studied in rabbit eyes, using light and electron microscopy. Glial cell extensions grew initially on the retinal surface around the wound site. This brief period of glial proliferation was associated with the posttraumatic inflammatory response and, more specifically, with phagocytic monocyte accumulation at the vitreoretinal interface. Once the inflammation subsided, this abortive attempt to grow membranes on the retinal surface stopped and true epiretinal membranes did not develop. Our observations suggest that intraocular inflammation and macrophage response determine the extent of healing and scarring on an injured retinal surface, and thus may play a key role in the pathogenesis of epiretinal membranes.

Animals↗