Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Retinal Pigments”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 127 records · Page 7Linked to original sources
PubMed2001

Comparative analysis of the uptake and expression of plasmid vectors in human ciliary and retinal pigment epithelial cells in vitro.

The retinal pigment epithelium is uniquely suited to gene therapy that uses lipid-mediated DNA transfer due to its high phagocytic activity in situ. We compared the relative efficacy of phagocytosis on the uptake of labeled plasmid vectors by retinal pigment epithelial and ciliary epithelial cells in vitro. Relative levels of endocytosis were then compared with the efficiency of marker transgene expression in these cells. Human retinal pigment epithelial and ciliary epithelial cells from a single donor were isolated and expanded in vitro. Polyplex-mediated transfections were performed using a rhodamine-labeled expression vector for green fluorescent protein. Rhodamine-labeled endosomes were examined by fluorescence microscopy at different time points. Rhodamine labeling and green fluorescent protein expression were analyzed by flow cytometry 48 h after transfection. These gene transfer studies showed that expression of transgenes does occur in both human retinal pigment epithelial and ciliary epithelial cells in vitro. Endocytosis of labeled plasmid vectors occurs at a significantly higher number and density in retinal pigment epithelial cells than in ciliary epithelial cells (P < 0.04). However, the efficiency of marker transgene expression is similar in the two cell types. These studies demonstrate that the higher intrinsic phagocytic activity does not enhance the efficacy of transgene expression in retinal pigment epithelial cells in vitro. Both human retinal pigment epithelial and ciliary epithelial cells are competent recipients for lipid-mediated gene transfer, and transgene expression occurs at similar levels in both cell types.

Animals↗
PubMed2001

Variegated expression and delayed retinal pigmentation during development in transgenic mice with a deletion in the locus control region of the tyrosinase gene.

Deletion of the tyrosinase locus control region (LCR) in transgenic mice results in variegated expression in the skin. Here we investigate the pigmentation pattern of other tissues that express tyrosinase: iris, choroid, and retina in the same animals. A mosaic distribution of pigmentation appears in the iris and choroid. Interestingly, a markedly different mosaic pattern is found in the retina, where central areas contain little or no melanin while pigmentation rises to normal levels towards periphery. Further, there is a temporal delay in the initiation and accumulation of pigment in retinal pigmented epithelium (RPE) cells during development, and patterns of adult retinal melanisation in these mice appear arrested at a stage found in early embryogenesis in wild-type mice. These results demonstrate that the tyrosinase LCR is needed for the correct establishment and maintenance of this expression domain throughout development, but particularly during the later stages of retinal melanisation.

Alleles↗
PubMed1987

Functional recovery of retinal pigment epithelial damage in experimental retinal detachment.

The integrity of the RPE barrier function in retinal detachment was studied in vitro. The retinal pigment epithelium (RPE)-choroid tissue was isolated from cynomolgus monkey eyes with acute (less than 1 hr), subacute (1-2 weeks), and chronic (8-20 months) retinal detachments, and clamped between Ussing-type chambers. Electrical characteristics and choroid-to-retina permeability to carboxyfluorescein were determined. In the HEPES-buffered bathing solution, transepithelial potential difference and resistance in eyes with acute retinal detachments (0.2 mV and 134 ohm-cm2, respectively) were significantly lower than subacute (7.9 and 350) and chronic (10.4 and 348) retinal detachments. Furthermore, the permeability was increased five-fold in acute retinal detachments with respect to subacute and chronic retinal detachments, indicating a breakdown of the RPE barrier in acute retinal detachment. No statistical difference was found between subacute and chronic retinal detachments. In this animal model, RPE barrier function is destroyed at the onset of retinal detachment, but recovers in a week or two, and is maintained in the chronic stage. Histological examination revealed that RPE recovery was accomplished by RPE proliferation and hyperplasia.

Animals↗
PubMed1983

Retinomotor pigment migration in the teleost retinal pigment epithelium. II. Cyclic-3',5'-adenosine monophosphate induction of dark-adaptive movement in vitro.

The retinal pigment epithelium (RPE) and photoreceptors of teleosts exhibit dramatic examples of cell motility (called retinomotor movements) in response to diurnal changes in lighting conditions. In darkness the pigment granules of the RPE migrate to the scleral base of the RPE cell and cone photoreceptors elongate. In the light these movements are reversed; pigment granules disperse into the long apical projections of the RPE cell and cones contract. It is reported here that treatments that elevate cytoplasmic cyclic AMP induce dark-adaptive movements (pigment aggregation and cone elongation) in light-adapted retinas cultured in the light. Treatments designed to elevate cGMP had no effect. In dose-response studies with the cAMP analog, dibutyryl cyclic AMP (dbcAMP), we found that the RPE pigment did not exhibit intermediate states of aggregation with increasing concentrations of dbcAMP but instead changed abruptly from the fully light-adapted to the fully dark-adapted retinomotor positions between 10 microM and 50 microM exogenous dbcAMP concentrations. Cones, on the other hand, elongated to intermediate extents in proportion to increasing dbcAMP concentration between 10 microM and 500 microM. These observations suggest that cytoplasmic cAMP plays a role in regulating retinomotor position in both RPE and cones.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Glycosaminoglycan degradation by cultured retinal pigment epithelium from patients with retinitis pigmentosa.

Patients with certain systemic deficiencies in the degradation of glycosaminoglycans (GAGs) often suffer from a retinal degeneration similar to that seen in retinitis pigmentosa. This applies to mucopolysaccharidosis (MPS) types I, II, and III, but not to type VI. The retinal pigment epithelium (RPE) is thought to contribute significantly to the synthesis and degradation of proteoglycans in the interphotoreceptor matrix. This raises the possibility that a defect in the synthesis or degradation of GAGs by the RPE may be related to some forms of retinal degeneration. In the present work, RPE from normal and RP donors was investigated for the capacity to correct deficiencies in GAG degradation by cultured skin fibroblasts from patients with different forms of MPS. A cross-correction technique was used in which abnormal increases in the incorporation of 35S-sulfate into GAGs by MPS fibroblasts was measured in the absence or presence of RPE cultures. RPE from normal donors corrected the defects in GAG degradation of fibroblasts from patients with MPS I, II, and III, but not MPS VI. The RPE from four donors with retinitis pigmentosa (one autosomal dominant, one sex-linked, and two isolated cases) and one donor with an unclassified isolated retinal degeneration demonstrated the same capacities to correct the MPS deficiencies as did normal RPE. Therefore, although retinitis pigmentosa is a heterogeneous disorder with several possible etiologies, no evidence was found in these five patients for a defect in GAG degradation that resembles the deficiencies of MPS patients.

Adult↗
PubMed1987

Fine structural significance of bone corpuscle-shaped pigmentation in the human retinal pigment degeneration.

Two cases of advanced RPD were observed their trypsin digested vascular trees and retinal substructures, especially RPE and pigmented cells in the neural retina. In the both eyes the visual cell was almost completely degenerated to disappear except posterior regions and apical part of RPE came to contact with neural retina or external limiting membrane formed by tight junction between adjacent Müller cell processes. Occasionally RPE in the equatorial region had completely disappeared and was replaced by Müller cell processes which was directly apposed to the Bruch's membrane. Pigmented cells were observed at almost all levels of the neural retina and along the intraretinal capillary. Pigmented cells were classified into three types. The first type of the cell was corresponded with the macrophage in the substructural features. The second type of the cell was RPE proliferated or migrated into the neural retina forming bone corpuscle-shape pigmentation in the retina and along the intraretinal capillary. Müller cell processes also indicated up-taking pigment granules, that is, the third type of the pigmented cell.

Adult↗
PubMed1985

Retinal pigment epithelial correlates of avian retinal degeneration: electron microscopic analysis.

The delayed amelanotic (DAM) strain of domestic chicken is characterized by an early, developmental onset of choroidal inflammation and destruction of both feather and choroidal melanocytes. Secondarily, retinal pigment epithelial (RPE) cells in the peripapillary region develop abnormalities, and a series of progressive histopathological changes ensues which includes reduction and ultimate loss of RPE-melanin granules and RPE-cell atrophy. The earliest sign of RPE-cell abnormality is a dramatic alteration in the distribution of intracellular melanin granules. Apical processes also show a lessening of contact with photoreceptor outer segments, leading in more advanced stages to their retraction and development of retinal detachments. Other progressive alterations in RPE cells include disorganization and loss of basal infoldings; size reductions and density increases in both mitochondria and myeloid bodies from early to advanced stages; appearance of large macrophages in the subretinal space; Loss of intercellular junctional complexes; and progressive reduction in the density of melanin granules. These abnormalities appear to spread in a cell-by-cell, radial pattern, until widespread areas of the retina become severely pathologic and atrophic. The DAM chorioretinal disorder appears to show many of the histopathologic features which characterize experimentally induced uveitis and other ocular diseases which may result from hypersensitivity to, or autoimmune reaction against, pigments of the uveal tract.

Animals↗
PubMed1985

An improved method for isolation and culture of rat retinal pigment epithelial cells.

Retinal pigment epithelial cells from normal, Long Evans (LE) and retinal dystrophic (RCS) rats can be grown in vitro (Edwards, 1977). An improved technique is described which permits a more rapid isolation of RPE cells, and routinely gives high cell yields (30,000-40,000/eye), excellent cell viability (95%), and high plating efficiencies (95-100%). Whole eyes are treated with hyaluronidase and collagenase followed by trypsin. These enzymes degrade components of the extracellular matrix, releasing sheets of RPE from adherent attachments to the retina and choroid. Trypsin was then used to dissociate the sheets into single cells. RPE cells are grown to confluence in primary culture. This technique permits RPE cell isolation from both normal and retinal dystrophic (RCS) rats, 8-15 days of age. Normal cells isolated by this technique consistently show excellent phagocytosis in vitro.

Animals↗
PubMed1997

CD36 expression is altered in retinal pigment epithelial cells of the RCS rat.

The retinal pigment epithelial cell has several important functions, one of which is the phagocytosis of photoreceptor outer segments which are discarded diurnally. We previously provided evidence in human retinal pigment epithelium that CD36, an 88 kDa integral membrane glycoprotein, participates in the phagocytosis of photoreceptor outer segments. Since in the Royal College of Surgeons dystrophic rat, retinal pigment epithelial cells fail to perform this function and as a result the photoreceptor cells degenerate, the expression of CD36 has now been examined by retinal pigment epithelial cells of the dystrophic rat. Consistent with earlier work using human retinal pigment epithelial cells, expression of CD36 by freshly isolated retinal pigment epithelial cells of Long Evans rats was confirmed by immunoblotting and immunocytochemistry with antibody to rat CD36. The protein was also present in lysates of cultured retinal pigment epithelium. Furthermore, with an in vitro phagocytosis assay using 125I-labeled outer segments, it was demonstrated that the binding and ingestion of outer segments by rat retinal pigment epithelial cells was reduced by 64% in the presence of antibodies to rat CD36. In contrast to observations in the Long Evans rat, immunoblotting of retinal pigment epithelial cells isolated from the adult Royal College of Surgeons rat revealed that CD36 protein was not present. This appeared to be a tissue-specific absence since CD36 protein was present in peritoneal macrophages harvested from the adult Royal College of Surgeons rat. A developmental study of CD36 expression also demonstrated an absence of the protein on the day of birth and at 1 and 2 weeks postnatally. By reverse transcriptase-polymerase chain reaction, CD36 mRNA was detected in freshly harvested retinal pigment epithelial cells of the Royal College of Surgeons rat at only PN1, 1 week and 10 days. Significantly, at 2 weeks of age and in the adult Royal College of Surgeons rat. CD36 transcripts were no longer present. Nevertheless, by Northern blot analysis CD36 mRNA was detected in various other tissues shown previously to express CD36. We conclude that in RPE cells of the Royal College of Surgeons rat, CD36 protein is not expressed while CD36 mRNA is present only transiently during postnatal development.

Animals↗
PubMed1996

Blue and ultraviolet light-absorbing opsin from the retinal pigment epithelium.

The retinal pigment epithelium (RPE) contains an abundant opsin that is distinct from rhodopsin and cone visual pigments and is able to bind the retinaldehyde chromophore. The putative retinal G protein-coupled receptor (RGR) was isolated in digitonin solution from bovine RPE microsomes and copurified consistently with a minor 34-kDa protein. The absorption spectrum of RGR revealed endogenous pH-sensitive absorbance in the blue and near-ultraviolet regions of light. Membrane-bound RGR was incubated with exogenously added all-trans-retinal and formed two long-lived pH-dependent photopigments with absorption maxima of 469 +/- 2.4 and 370 +/- 7.3 nm. The effects of hydrogen ion concentration suggest that the blue and near-UV photopigments are tautomeric forms of RGR, in which an all-trans-retinal Schiff base is protonated or unprotonated, respectively. The RPE pigment was also demonstrable by its reactivity to hydroxylamine in the dark. The retinaldehyde-RGR conjugate at neutral pH favors the near-UV pigment and is a novel light-absorbing opsin in the vertebrate eye.

Animals↗
PubMed1975

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↗
PubMed1986

Experimental diabetes mellitus impairs the function of the retinal pigmented epithelium.

The retinal pigmented epithelium (RPE), which influences the composition of the retinal extracellular fluid, is significantly affected in diabetes. Changes in RPE morphology, permeability, and electrophysiology in experimentally diabetic animals have been described. To facilitate the study of diabetes-related changes in RPE metabolism, we applied the techniques of quantitative histochemistry to pure samples of RPE and individual retinal layers from eyes of normal and alloxan-diabetic rabbits. Glucose within the RPE approximated serum levels in both normal and diabetic animals. Other changes in diabetics included increased sorbitol, decreased myo-inositol, elevated total Na, and loss of measurable Na+-K+-ATPase activity within the RPE. The altered ion metabolism was associated with a progressive decrease in the amplitude of the RPE-generated c-wave of the electroretinogram. The deterioration of the c-wave was arrested by treatment of the diabetic animals with either myo-inositol supplementation or with sorbinil, an inhibitor of aldose reduction. Diabetic alterations in the RPE might impair the ability of the tissue to maintain normal transport functions. The subsequently altered composition of the extracellular environment of the retina may play an important role in the pathogenesis of diabetic retinopathy.

Animals↗
PubMed1996

Pattern dystrophies of the retinal pigment epithelium.

Pattern dystrophies of the retinal pigment epithelium are infrequent fundus abnormalities arranged in various patterns of dots, lines and branches. The basic lesion appears to be yellow deposits of abnormal lipofuscin accumulated within degenerated retinal pigment epithelium cells. Examinations were carried out on two families who had developed different patterned alterations in the retinal pigment epithelium. The proband of family 1 had diffuse changes associated with equatorial folds. One sister had a macular alteration. A daughter was normal; a son had bilateral atrophy of the temporal retinal pigment epithelium. The proband of family 2 had bilateral, symmetrical retinal pigment epithelium lesions that simulated fundus flavimaculatus. His first daughter had a central lesion in her right eye. The second daughter, a peripapillary crescent of hyperpigmentation in her right eye, and circumpapillary chorioretinal atrophy associated with foveolar abnormalities in the left. This report provides further evidence that variable types of pattern dystrophy can occur within a single family pedigree and support the current opinion that all forms of pattern dystrophies are variants of a single pathogenic mechanism.

Adult↗
PubMed1989

Cytomegalovirus replication in cultured human retinal pigment epithelial cells.

Retinal pigment epithelium (RPE) was isolated from the globe of a donor positive for human immunodeficiency virus (HIV) who had cytomegalovirus (CMV) retinitis secondary to acquired immunodeficiency syndrome (AIDS). In culture, the cells exhibited normal epithelioid morphology by phase contrast microscopy. After two weeks the cells developed cytomegaly and dense intranuclear and cytoplasmic inclusions and, eventually, died. Transmission electron microscopy (EM) demonstrated intranuclear nonenveloped virus particles 80-120 nm in diameter consistent with a herpes type infection. Immunofluorescence staining demonstrated the presence of CMV antigens. Conditioned medium from the infected cells caused infection in RPE cells isolated from normal donors. Hybridization assay demonstrated the presence of CMV DNA and indicated that the time course of the infection was similar, but not identical to infection in MRC-5 and HEL cells. We conclude that cultured human RPE is a permissive host for CMV.

Acquired Immunodeficiency Syndrome↗
PubMed1992

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↗
PubMed1985

Culture of retinal pigment epithelium from chorio-retinal biopsies.

The recently devised methods for surgical sampling of chorio-retinal tissue permits morphological evaluation of retina in various diseases. In the present report it is demonstrated, that the retinal pigment epithelium in such samples can be isolated as a viable cell population, and that the cell mass can be increased sufficiently in culture to permit biochemical as well as morphological studies. This procedure thereby expands the diagnostic potential of the sample tissue.

Animals↗
PubMed1993

Fibroblast growth factor receptor deficiency in dystrophic retinal pigmented epithelium.

The retinal pigmented epithelium (RPE) is known to be the site of the primary lesion in inherited retinal dystrophy in the Royal College of Surgeons (RCS) rat, a model for retinitis pigmentosa. Although the only functional defect so far detected in these cells is their failure to efficiently phagocytose shed photoreceptor outer segment debris, the actual cause of photoreceptor cell death is still unknown. Recently the possibility of "trophic factors" important in photoreceptor survival produced by normal RPE but not by dystrophic RPE has been suggested. Hence we decided to investigate the presence and abundance of two candidate diffusible factors, the acidic and basic fibroblast growth factors (aFGF and bFGF, respectively), as well as their high affinity cell surface receptors (FGF-R). mRNA was isolated from primary cultures of purified normal and dystrophic RPE and analyzed by PCR amplification using specific oligonucleotide primers for aFGF and bFGF: the size and abundance of amplified fragments was similar for both cell types. Also, aFGF protein, detected by immunocytochemistry using specific antisera, appeared to be present in approximately equal amounts and distributed in a similar pattern. However, scatchard analysis of radio-labelled bFGF binding to primary cultures of normal and dystrophic rat RPE revealed that dystrophic RPE possess only 29% the number of surface receptors compared to congenic normal cells. Furthermore, the level of expression of FGF-R2 mRNA, but not that of FGF-R1, was significantly different. Other parameters measured (receptor affinity, profile of ligand internalization and degradation, receptor molecular weight and mitogenic activity) did not show any significant differences between normal and dystrophic RPE. The precise role of FGF-R deficiency in the etiology of the disease hence remains to be determined, but it indicates the importance of trophic factors in the normal functioning of the retina.

Animals↗
PubMedDate not supplied

Scleral indentation following cryotherapy and repeat cryotherapy enhance release of viable retinal pigment epithelial cells.

Retinal pigment epithelial (RPE) cells are an important component of intravitreal and epiretinal membranes in proliferative vitreoretinopathy (PVR) that contract and cause recurrent retinal detachment. Cryotherapy has been shown to enhance release of viable RPE cells into the vitreous cavity. This study demonstrates that repeat cryotherapy (refreezing) releases viable RPE cells in even larger numbers. Repeated indentation of the sclera after transscleral cryotherapy also releases more viable RPE cells than does cryotherapy alone or scleral indentation preceding cryotherapy. These findings suggest that refreezing should be avoided, and repeated indentation of the sclera should be minimized after cryotherapy.

Animals↗