PubMed HealthSearch

SEARCH · PubMed Health

Results for “Retinal Pigments”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Preserved para-arteriolar retinal pigment epithelium retinitis pigmentosa.

In two patients, we studied retinitis pigmentosa with preservation of the retinal pigment epithelium adjacent to and under the retinal arterioles (despite panretinal degeneration). Both patients with preserved para-arteriolar retinal pigment epithelium also exhibited a peculiarly strong hyperopia. In addition to previously reported features, these patients also had sheathing of the major vascular arcades, which suggested a vascular involvement in this uncommon form of retinitis pigmentosa.

Adult

Ultrastructural and immunocytochemical changes in retinal pigment epithelium, retinal glia, and fibroblasts in vitreous culture.

Retinal pigment epithelial (RPE) cells, retinal glial, and fibroblasts, three cell types believed to play a role in the pathogenesis of epiretinal membrane formation, were maintained in vitreous culture to determine the influence of vitreous on their ultrastructure and expression of cytokeratin, glial fibrillary acidic protein (GFAP), vimentin, and glutamine synthetase (GS). Using a highly sensitive, preembedding technique for the immunolocalization of these antigens at the ultrastructural level, most RPE cells were found to lose cytokeratin and vimentin within 1 day after seeding on irradiated vitreous. The percentage of keratin-positive cells then increased with time in culture. If the vitreous was placed on RPE cells cultured in monolayer instead of placing the cells on the vitreous, keratin and vimentin were expressed these intermediate filament proteins diminished with time. Glutamine synthetase was found in RPE cells grown in monolayer with or without a vitreous overlay, but not in RPE cells grown on the surface of vitreous. Retinal glial grown on vitreous showed a time-dependent decrease in the number of cells expressing GFAP and a corresponding increase in cells expressing vimentin or GS. Some fibroblasts in vitreous culture expressed vimentin but not the other antigens evaluated. A substantial number of cells in each culture did not stain positively for cytokeratin, GFAP, vimentin, or GS. All three cell types showed phenotypic diversity at the ultrastructural level with each cell type being capable of assuming the same morphologic appearance under certain conditions. These results demonstrate the phenotypic plasticity of RPE cells, retinal glia, and fibroblasts when grown in contact with vitreous and provide further evidence that neither ultrastructure, intermediate filament protein expression, nor the presence of GS is sufficient to determine the cell type of origin of cells in epiretinal membranes.

Animals

Fluorescent pigment accumulation in retinal pigment epithelium of antioxidant-deficient rats.

A yellow autofluorescent pigment, generally thought to be indicative of membrane autoxidation, was found to accumulate in the retinal pigment epithelium (RPE) of rats maintained for 32 weeks on diets producing physiological antioxidant deficiency. The largest build-up of fluorescent pigment occurred in rats fed a diet high in polyunsaturated fatty acids (PUFAs) and deficient in alpha-tocopherol (vitamin E), selenium, sulfur-containing amino acids, and chromium. These latter four nutrients have all been implicated in maintaining the antioxidant status of tissues, whereas PUFAs are pro-oxidants. Dietary supplementation with methionine and chromium significantly reduced the amount of fluorescent pigment accumulated in the RPE. Supplementation with all four nutrients further reduced the amount of fluorescent pigment to a very low level. Rats maintained on a normal laboratory diet, relatively low in PUFAs and presumably adequate in other nutrients, accumulated relatively small amounts of fluorescent pigment in the RPE. Of all tissues in the retina and choroid, the autofluorescent pigment was found to be almost entirely restricted to the RPE. The autofluorescence produced in the RPE by antioxidant deficiency was more concentrated than that produced in the testes, kidney, intestine, and heart. This suggests that the RPE is particularly sensitive to physiological antioxidant deficiencies. The increased fluorescent pigment build-up in the RPE of antioxidant-deficient rats appears to correlate with a decreased RPE melanin content. Similar changes in pigmentation have been reported to occur in human RPE with age and in dominantly inherited retinitis pigmentosa. Thus, with respect to its effect on RPE pigmentation, antioxidant deficiency appears to mimic aging and possibly some aspects of one type of retinitis pigmentosa.

Amino Acids, Sulfur

Observations on the retinal pigment epithelium and retinal macrophages in experimental retinal detachment.

After experimental retinal detachment in rabbits macrophages are a prominent feature in the subretinal space or within the retina. Two sources for these macrophages are identified. The retinal pigment epithelium (RPE) may undergo metaplasia and actively 'bud'; the evolving macrophage is then formed by a vitreal protrusion of the cytoplasm of an RPE cell which is 'nipped off' by lateral protrusions from adjacent cells. In addition, in regions of RPE proliferation, blood-borne cells were found in Bruch's membrane and among the mass of proliferated RPE cells, suggesting that blood-borne cells may pass from the choroidal circulation through Bruch's membrane and the RPE layer.

Animals

Modulation of potassium transport in cultured retinal pigment epithelium and retinal glial cells by serum and epidermal growth factor.

The ionic environment of retinal photoreceptors is partially controlled by potassium transporters on retinal glial and retinal pigment epithelial cells (RPE). In this study, serum and epidermal growth factor (EGF) were examined as modulators of potassium transport in confluent cultures of human RPE and rabbit retinal glia. EGF is a known mitogen for confluent RPE cultures and was shown here to also stimulate [3H]thymidine incorporation in cultures of retinal glia. For potassium transport studies 86Rb was used as a tracer during a 17-min incubation. For both retinal cell types the mean total 86Rb uptake in 10% serum was approximately 60% above basal, serum-free controls. For EGF, tested in several experiments in a concentration range from 1 to 100 ng/ml, maximal total uptake was 33 and 24% above controls for RPE and glia, respectively. Inhibitor studies suggested that basal and serum-stimulated uptake for both cell types occurred by the ouabain-sensitive Na-K ATPase pump and by the furosemide- or bumetanide-sensitive Na-K-Cl cotransporter. EGF-stimulated uptake appeared to be due predominantly to the cotransporter. The data suggest that serum components and EGF, which may be available to retina-derived cells under pathologic conditions, may not only stimulate proliferation but may also act as short-term modulators of potassium ion movement and thus affect physiologic processes that are sensitive to ion homeostasis.

Animals

[Krypton laser therapy. Use in secondary serous detachment of the retinal pigment epithelium and in multiple idiopathic serous detachments of the retinal pigment epithelium].

Two variants of serious detachments of the retinal pigment epithelium (RPE) are demonstrated with reports of typical cases: (1) secondary serous detachment of the RPE; (2) idiopathic serous detachment of the RPE (pigment epithelium detachment not associated with any other retinal or choroidal disease). Fluorescein angiographic criteria for differential diagnosis and the resulting different techniques of krypton laser coagulation are portrayed: (a) focal krypton laser coagulation of the total area of the pigment epithelium detachment; (b) circular, one-row laser coagulation at the detachment borders. The advantages of circular, one-row laser coagulation of idiopathic serous RPE detachment over coagulation of the total area of the RPE detachment are described: first, these are fewer scotomas following coagulation; second, fewer laser foci are required; and third, the risk of subretinal bleeding is lower. These findings emphasize the efficiency of circular, one-row laser coagulation at the detachment borders in the treatment of idiopathic serous RPE detachments.

Adult

Effects of colchicine on phagosome-lysosome interaction in retinal pigment epithelium. II. In vitro observations on histio-organotypical retinal pigment epithelial cells of the pig (a preliminary report).

Phagocytic activity of histiotypical and organotypical retinal pigment epithelial cells was studied by SEM and EM. After a latent period polystyrene microspheres of different diameter were captured by newly formed microvilli. No mechanism of discrimination according to the size of microspheres was observed. After engulfment, microvilli of histiotypical cells decreased in length and finally disappeared. Lysosomes increased in number when compared to unstimulated cells and fused with many latex-containing phagosomes. Colchicine, when added at 5 X 10(-5) M to the medium, inhibits phagosome-lysome interaction, thus confirming in vivo observations.

Animals

Retinal pigment epithelial degeneration, partial retinal atrophy and macular hole in acute lymphocytic leukemia.

A seven year old child with acute lymphocytic leukemia presented at autopsy with a macular hole, and degeneration of the retinal pigment epithelium and its overlying photoreceptors. She had been treated with cobalt 60, methotrexate, vincristine cyclophosphamide and prednisone. A review of the literature of similar findings as well as pigment epithelial degenerations from other causes is presented.

Antineoplastic Agents

Experimental autoimmune anterior uveitis (EAAU). II. Dose-dependent induction and adoptive transfer using a melanin-bound antigen of the retinal pigment epithelium.

Retinal pigment epithelial cell fractions have been investigated for their capacity to induce experimental uveitis. Cells of the dark (melanotic) and light areas of the bovine RPE have subsequently been extracted by buffer, Triton X-100, sodium dodecyl sulfate (SDS), and treated with various reagents in order to study some characteristics of the antigen. The SDS-insoluble melanotic fraction, consisting of spindle-shaped, mature melanin granules, proved to be the most uveitogenic preparation. Using pertussis toxin as coadjuvant, 1 microgram of melanin-protein (3.4 x 10(6) granules) was able to induce experimental autoimmune anterior uveitis (EAAU) in Lewis rats. The pathogenic activity of the responsible pathogen (PEP-X) was not diminished by SDS, nor eliminated by mildly alkaline SDS or formic acid treatment. However, HCl-deproteinized granules were not uveitogenic. The results show that PEP-X is a highly stable melano-antigen that is probably covalently bound to the granule surface. This is the first time that a melanin-bound antigen has been demonstrated to evoke specific autoaggressive activity. EAAU could adoptively be transferred by sensitized and in vitro stimulated CD4 T-lymphocytes. The evoked inflammation started 3-4 days after injection, was similar to those induced by immunization, and consisted mainly of severe iridocyclitis accompanied by dense flare and cells in the anterior chamber. Choroiditis developed in severe cases of EAAU but no inflammation was detected in the retina, pineal gland or other organs of these rats. EAAU could not be transferred by serum. Immunized PVG rats and guinea-pigs did not develop ocular inflammation. In monkeys a high dose of antigen evoked a very mild EAAU accompanied by choroiditis. In view of its characteristics, EAAU may be a new model for human anterior uveitis.

Animals

Bilateral recurrent acute retinal pigment epitheliitis.

Acute retinal pigment epitheliitis appears to be a specific discrete process of unknown etiology. It is generally unilateral but can be recurrent and can affect both eyes. Eyes in which the disease has run its course exhibit little or no unusual ophthalmoscopic or visual function abnormalities. The actue phase of the disease is localized to the macular area. The lesions are localized in the retinal pigment epithelium as shown by slit-lamp and contact-lens examination, the small lesions more or less surrounding the fovea. They vary from tiny grayish to black spots, which may become surrounded by a lighter halo. Fluroescein angiography is normal in acute phases but the halo-like areas may represent "window defects" with hyperfluorescence in later stages.

Adolescent

[Pigmentation of feather primordium achieved by grafting of retinal pigment epithelium].

Small fragments of the retinal pigmented epithelium from White Leghorn, Rhode Island Red chick embryos, and from Quail, Starling and Red Partridge embryos, were grafted into the wing bud of White Leghorn chick embryos. Retinal pigmented epithelium of White Leghorn chick embryos did not give rise to pigmentation of feather primordia in the hosts. In contrast, 60% of grafts from Rhode Island Red, Quail, Starling and Red Partridge, gave rise to feather primordia whose pigmentation was identical to that of the donors. Pigmentation depends on the fact that some graft retinal melanocytes diffuse in the wing bud of the host and reach the feather primordia. This was shown by the Feulgen technique in embryos grafted with Quail retinal pigmented epithelium, taking advantage of the fact that Quail cells possess DNA rich nucleoli. The local factors which allow the migration of the melanocytes are probably inactive on the retinal melanocytes of the White Leghorn chick embryos, whose genotype does not contain the "feather pigmentation" character.

Animals

The occurrence of actinlike filaments in association with migrating pigment granules in frog retinal pigment epithelium.

In the retina of the frog and certain other animals, melanin pigment granules move in response to light so as to shield photoreceptor outer segments. The granules are contained within the cells of the pigment epithelium (PE) which lie as a continuous sheet between the neural retina and the choroid. Moderate illumination of the eye causes the melanin granules to move from a region within a PE cell body into numerous fingerlike extensions of the cell which interdigitate with the receptor outer segments. This migration takes many minutes and is reversed when the light falling on the eye increases in intensity. Several reviews are concerned with the early descriptions of this phenomenon (6,30) and with more recent experiments (1,5,19). The mechanism of the pigment granule motion is undetermined although there are studies concerning PE ultrastructure (8, 23, 31), scanning electron microscopy of the fingerlike extensions of the PE cells (27), the role of the PE in photoreceptor phagocytosis (32), the nature of the pigment granules (19), and the action spectrum of the light which induces the migration (16). This study reports the presence of a system of microfilaments associated with the pigment granules in the fingerlike extensions processes of the PE cells. We demonstrate by heavy meromyosin (HMM) labeling that the filaments are actinlike in character and suggest that these filaments could be responsible for the migration of the melanin pigment granules.

Actins

Release of iron by human retinal pigment epithelial cells.

Retinal pigment epithelial cells, which form one aspect of the blood-retinal barrier, take up iron in association with transferrin by a typical receptor-mediated mechanism (Hunt et al., 1989. J. Cell Sci. 92:655-666). This iron is dissociated from transferrin in a low pH environment and uptake is sensitive to agents that inhibit endosomal acidification. The dissociated iron enters the cytoplasm as a low molecular weight (less than 10 kD) component and subsequently binds to ferritin. No evidence for recycling of iron in association with transferrin was found. Nevertheless, much of the iron that is taken up is recycled to the extracellular medium, primarily from the low molecular weight pool. This release of iron is not sensitive to inhibitors of energy production or of vesicular acidification but is increased up to a maximum of about 40% of the total 55Fe incorporated when cells are incubated with serum or the medium is changed. When a short loading time for 55Fe from 55Fe-transferrin is used (i.e., when the low molecular weight pool is proportionately larger), a much larger fraction of the cell-associated radiolabel is released than when longer loading times are used. The data suggest that a releasable intracellular iron pool is in equilibrium with the externalized material. The released iron may be separated into a high and a low molecular weight component. The former is similar on polyacrylamide gel electrophoresis to ferritin although it cannot be immune precipitated by anti-ferritin antibodies. The low molecular weight 55Fe which is heterogeneous in nature can be bound by external apo-transferrin and may represent a form that can be taken up by cells beyond the blood-retinal barrier.

Biological Transport

Polarized budding of vesicular stomatitis and influenza virus from cultured human and bovine retinal pigment epithelium.

The retinal pigment epithelium (RPE) is able to perform a variety of functions because of its high degree of plasma membrane polarity. Some aspects of this polarity such as the localization of the majority of Na-K ATPase to the apical membrane distinguish the RPE from kidney cells and most other transporting epithelia. The polarized budding of enveloped viruses such as vesicular stomatitis and influenza from the basolateral and apical membrane, respectively, has been used to study mechanisms underlying the domain-specific sorting of membrane proteins in cultured epithelial cell lines. These processes also serve as a useful index of the degree of polarization in epithelial cell cultures. Viral budding from apical and basolateral RPE membranes was used in this study to determine whether the sorting of viral envelope membrane proteins by the RPE is reversed in polarity from that of kidney cells and, if so, whether this might predict a fundamental difference in membrane protein sorting for RPE. The results clearly indicate that the polarity of viral membrane sorting and subsequent viral budding is the same in RPE as in other polarized epithelial cell lines examined to date.

Animals

Interleukin-6 (IL-6) gene expression and secretion by cytokine-stimulated human retinal pigment epithelial cells.

Retinal and choroidal inflammatory lesions are important causes of visual loss, but the mechanisms regulating intraocular inflammation remain poorly understood. By virtue of its position at the blood-retina barrier, the retinal pigment epithelium (RPE) cells may be critical to the initiation and propagation of ocular inflammation. Previously we showed that cytokine-stimulated RPE cells produce interleukin-8, a well-defined chemotactic factor for neutrophils and lymphocytes. In this study, we found that human RPE cells stimulated by human recombinant interleukin-1-beta (rIL-1 beta) or tumor necrosis factor-alpha (rTNF-alpha) produce interleukin-6 (IL-6). Using a plasmacytoma proliferation assay, significant levels of IL-6 were found in media of RPE cells stimulated with either rIL-1 beta or rTNF-alpha for 4 hr. Progressive accumulation of IL-6 in media overlying stimulated RPE cells occurred over the subsequent 20 hr. IL-1 beta was a significantly more potent stimulator of RPE IL-6 production than TNF-alpha, RPE IL-6 production in response to each of these cytokines was also dose-dependent over a range of 20 pg to 20 ng ml-1. Specific anti IL-6 antibody, but not control immunoglobulin, neutralized RPE-derived IL-6 activity in the plasmacytoma proliferation assays. RPE IL-6 mRNA levels were detectable 1 hr after cytokine stimulation, plateaued within 8 hr in 24-hr assays, and demonstrated dose-dependent kinetics in 6 hr assays. Lipopolysaccharide failed to induce RPE IL-6 mRNA expression or RPE IL-6 production.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence