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PubMed1993

Immortalization of polarized rat retinal pigment epithelium.

Rat retinal pigment epithelial (RPE) cells were immortalized by infection with a temperature-sensitive tsA SV40 virus and following cloning and selection for epithelial properties the polarized RPE-J cell line was obtained. At the permissive temperature of 33 degrees C, RPE-J cells behave as an immortalized cell line. When RPE-J cells are grown on nitrocellulose filters coated with a thin layer of Matrigel in the presence of 10(-8) M retinoic acid for 6 days at 33 degrees C and then switched for 33-36 hours to the non-permissive temperature of 40 degrees C, they acquire a differentiated polarized RPE phenotype. Under these growth conditions, RPE-J cells exhibit circumferential staining for the tight-junction protein ZO-1 and acquire a transepithelial resistance of 350 ohms cm2. Morphologically, RPE-J cells exhibit a characteristic RPE morphology with extensive apical microvilli as well as numerous dense bodies including premelanosomes and varied multilamellar structures. Ruthenium red labeling revealed the frequent basal localization of the tight junction. The cells were identified to be of rat RPE origin by their expression of the rat RPE marker RET-PE2 and their ability to phagocytose latex beads. While RPE-J cells are capable of sorting influenza and vesicular stomatitis virus to the apical and basal surfaces, respectively, the Na,K-ATPase is not polarized and the neural cell adhesion molecule, N-CAM, is localized exclusively to the lateral surface. In vivo the apical surface of RPE interacts with the adjacent neural retina and the Na,K-ATPase and N-CAM are both apical; the altered polarity of these two proteins in RPE-J cells may be a consequence of the absence of apical interaction with the neural retina in culture. Previous studies of RPE have been restricted to the use of primary cultures and the RPE-J cell line should prove an excellent model system for the study of the mechanisms determining the characteristic polarity and functions of the retinal pigment epithelium.

Animals↗
PubMed2000

Dorsal retinal pigment epithelium differentiates as neural retina in the microphthalmia (mi/mi) mouse.

PURPOSE: Microphthalmia, a bHLH-zip transcription factor associated with the onset and maintenance of pigmentation, identifies the retinal pigment epithelial (RPE) compartment during optic vesicle and optic cup development. To determine a role for microphthalmia (mi) during eye development, the effects of an mi loss of function mutation on RPE and neural retinal were investigated in the mi/mi mouse. METHODS: A series of embryonic and postnatal mi/mi and wild-type eyes were sectioned and labeled with neural retina- and RPE cell type-specific antibodies. Photoreceptor loss was quantified by counting the number of photoreceptor nuclei spanning the outer nuclear layer throughout postnatal retinal development. RESULTS: Early neural retinal differentiation is not affected in the mi/mi mouse. The mi/mi ventral retinal pigment epithelial layer begins to develop normally, but does not pigment or attain a differentiated cuboidal morphology. The dorsal region of mi/mi retinal pigment epithelium expands and forms an ectopic retina, which develops all major retinal cell types along a similar time course as the wild type. After birth, mi/mi photoreceptors begin to form rosettes, outer segments fail to elongate, and over an extended time period, the retina degenerates. CONCLUSIONS: Together these results suggest that early retinal development can proceed normally in the mi/mi mutant, but later retinal histogenesis is dependent on the presence of a differentiated retinal pigment epithelium. Most importantly, loss of mi function permits a change in cell fate from RPE to retina in the dorsal eye.

Animals↗
PubMed1985

The focal adhesions of chick retinal pigmented epithelial cells.

Retinal pigmented epithelial (RPE) cells obtained from the eyes of chick embryos from colonies in vitro in which cells at the periphery of the colony express an undifferentiated, well-spread morphology and develop extremely large areas of cell-substratum adhesion. These adhesions can be classified as focal on the basis of the following: (a) their black surface reflection interference image, the contrast of which is not affected by changes in either the wavelength of the incident light or the refractive index of the immersion medium; (b) their association with the termini of actin-containing microfilament bundles; and (c) their ability to be labelled with antiserum against vinculin, a protein specific for adhesions of the focal type. The focal adhesions of RPE cells comprise laterally associated individual focal contacts, the mechanism by which this association is achieved and maintained is yet unknown. Because of the unusually large size and excellent microscopical definition of their focal adhesions, I used RPE cells to investigate the role of other actin-associated proteins in adhesion complexes. One of these, nonerythroid spectrin (fodrin), a protein suggested to play a role in anchoring actin filaments to the plasma membrane, was neither concentrated in nor excluded from the focal adhesions of RPE cells. Thus, at least in this cell type, spectrin seems unlikely to serve as a link between the major actin-containing microfilament bundles and the plasma membrane in the regions of cell-to-substratum contacts.

Actin Cytoskeleton↗
PubMed1983

The fate of the phagosome: conversion to 'age pigment' and impact in human retinal pigment epithelium.

Phagosomes are converted to phagolysosomes and then to residual bodies (also known as lipofuscin granules or age pigment). Lipofuscin granules of retinal pigment epithelial (RPE) cells of single human eyes were isolated and analysed for enzyme content and fluorescence spectra. The granules are low in lysosomal enzymes and they fluoresce yellow-gold. Thin layer chromatography reveals several separable constituents. Lipofuscin granules accumulate with age, the largest increase occurring after the first decade of life in humans. Macular RPE cells accumulate granules more than non-macular cells.

Adolescent↗
PubMed1978

[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↗
PubMed1988

Retinal pigment epithelial cells in culture produce retinal vascular mitogens.

Conditioned medium from human retinal pigment epithelial cells in culture significantly stimulated the proliferation of subcultured bovine retinal capillary endothelial cells, pericytes, and freshly isolated retinal microvessels. The vascular mitogenic activity enhanced that of retinal crude extract. No evidence emerged of an inhibitor of microvascular cellular proliferation produced by retinal pigment epithelial cells.

Animals↗
PubMed2003

UV irradiation causes multiple cellular changes in cultured human retinal pigment epithelium cells.

BACKGROUND: The retinal pigment epithelium maybe causally involved in the development and progression of age-related macula degeneration; however, the mechanisms leading to the development of age-related macula degeneration remain largely unknown. The purpose of this study was to examine cellular changes in the retinal pigment epithelium induced by direct irradiation with UV light in culture. METHODS: Retinal pigment epithelium cells from post-mortem human retinas were used to obtain dissociated cultures with cells retaining the ability to differentiate in vitro. These cells were cultured over several days to weeks. The UV radiation (UV-A and UV-B) occurred under sterile conditions with a 100 HBO/mercury bulb attached to a dissecting microscope, delivering co-axial illumination. The time dependence of irradiation effects was analysed using morphometric, immunohistochemical, functional and apoptosis-detecting techniques. RESULTS: Vital and proliferating retinal pigment epithelium cell cultures could be prepared consistently. The cells showed tissue-specific morphologies in vitro for several days to weeks. Pigment epithelium-derived factor was detected in these cells using immunocytochemistry and Western blots. The UV irradiation but not white light resulted in measurable alterations of cell shape and size. The irradiated cells showed partial swelling and shrinkage reminiscent of progressing apoptotic degeneration. TUNEL staining revealed that apoptosis was induced by UV light, but not detectably by white light. The phagocytosis of fluorescent micro-particles diminished after irradiation. These effects were dependent on the duration of irradiation. CONCLUSIONS: Cultures of retinal pigment epithelium are suitable and sensitive models to study cell damage and may contribute to unravelling the pathogenetic mechanisms of retinal degeneration.

Apoptosis↗
PubMed1995

Monocyte-induced cytokine expression in cultured human retinal pigment epithelial cells.

Monocytes and retinal pigment epithelial cells are intimately associated in membranes of eyes with proliferative vitreoretinopathy and in certain types of uveitis. The goal of this study was to determine whether monocytes modulate cytokine expression in retinal pigment epithelial cells, and if so, to identify the monocyte products responsible for this effect. Cultured human retinal pigment epithelial cells were exposed to varying concentrations of monocyte-conditioned medium from unstimulated human monocytes for 1-48 hr, or from monocytes prestimulated with lipopolysaccharide. mRNA expression of interleukin-1 beta, interleukin-6, interleukin-8, melanoma growth stimulating activity/gro alpha and gamma, macrophage colony stimulating factor, transforming growth factor-beta 2, basic fibroblast growth factor and activin beta A chain was determined by reverse transcription polymerase chain reaction. Protein secretion of selected cytokines, interleukin-1 beta, interleukin-6, interleukin-8, macrophage colony stimulating factor and transforming growth factor-beta 2 was measured in RPE-conditioned medium by ELISA. Retinal pigment epithelial cells constitutively expressed mRNA for interleukin-6, macrophage colony stimulating factor, transforming growth factor-beta 2, basic fibroblast growth factor and activin beta A chain. Interleukin-1 beta, melanoma growth stimulating activity/gro alpha and gamma and interleukin-8 were not expressed under basal conditions. Stimulated monocyte-conditioned medium markedly induced mRNA of all cytokines except basic fibroblast growth factor and transforming growth factor-beta 2 in a dose- and time-dependent manner. Unstimulated monocyte-conditioned medium was a less potent inducing agent, but still enhanced mRNA expression of interleukin-6, interleukin-8 and melanoma growth stimulating activity/gro alpha. Stimulated monocyte-conditioned medium also induced a time-dependent increase in interleukin-6, Interleukin-8, macrophage colony stimulation factor and transforming growth factor-beta 2, but not interleukin-1 beta protein secretion (p < 0.05 for all time points). Neutralizing antibodies to interleukin-1 beta, or tumour necrosis factor alpha, but not interleukin-1 alpha, significantly reduced cytokine mRNA expression induced by stimulated monocyte-conditioned medium. The combination of all three neutralizing antibodies almost entirely eliminated monocyte-induced mRNA expression and protein production of all cytokines studied. Activated monocytes secrete a heterogeneous mixture of products that together strongly induce expression of multiple cytokines in human retinal pigment epithelial cells. Most if not all of the inducing effect can be accounted for by interleukin-1 beta and tumour necrosis factor alpha. Because cytokines have been implicated in proliferative vitreoretinopathy and uveitis, monocyte-mediated cytokine expression by RPE cells may serve to initiate and perpetuate these diseases.

Antibodies↗
PubMed1983

Retinomotor pigment migration in the teleost retinal pigment epithelium. I. Roles for actin and microtubules in pigment granule transport and cone movement.

In lower vertebrates, retinal pigment epithelial (RPE) cells and photoreceptors undergo dramatic "retinomotor movements" in response to changes in light conditions. In the dark, RPE pigment granules aggregate to the (choroidal) base of the RPE cells, cones elongate, and rods contract. In the light, movements are reversed: pigment granules migrate out into the long apical projections of the RPE cells, cones contract, and rods elongate. In this report the time courses of dark-induced pigment aggregation and light-induced dispersion have been characterized (and compared to cone movements) in the blue stripe grunt, Haemulon sciurus. It was found that aggregation and dispersion occur at linear rates of 3.4-3.5 microns/min and that RPE movements are kinetically independent from cone movements induced by the same changes in light conditions. The roles of actin and microtubules in RPE and cone movements were also investigated by using the actin-inhibitors, cytochalasins-B and -D, and the microtubule inhibitor, colchicine. Light-induced pigment dispersion, as well as maintenance of the fully dispersed (light-adapted) position appear to require actin-dependent processes. Intraocularly injected cytochalasins-B and -D fully prevented pigment dispersion when administered to dark-adapted animals immediately prior to their exposure to light, and caused pigment aggregation to the RPE cell base when administered to fully light-adapted animals. Ultrastructural studies showed that actin filaments, which in untreated retinas were found closely associated with pigment granules and the plasma membrane, were disrupted after cytochalasin-B treatment. Both dispersive and aggregative pigment movements within the cell body appeared to require microtubule-dependent processes. Intraocularly injected colchicine disrupted microtubules and blocked pigment granule translocation in both directions in the cell body. A hypothetical model to explain pigment movements in response to changes in light conditions is proposed based on these observations as well as on data from the literature.

Actins↗
PubMed1993

Phagocytic and digestive activities of retinal pigment epithelium at experimentally produced retinal tears.

The present study examined the phagocytic and digestive activities of retinal pigment epithelial cells (RPE cells) at sites of experimentally produced retinal tears, using the phagocytosis of the latex particles by these cells as a measure of phagocytic activity, and their acid phosphatase activity as a measure of their digestive activity. Four days after retinal tear formation, acid phosphatase activity of RPE cells at the site of retinal tears was the same as that of the RPE cells in the surrounding normal retina. However, at one week, four weeks and six months after tear formation, acid phosphatase activity of RPE cells at the site of retinal tears was higher than that of the RPE cells in the surrounding normal retina. Four weeks after retinal tear formation, a latex particle solution was injected onto the retinal tear or subretinally. The RPE cells at the site of retinal tears phagocytized the latex particles earlier than did the RPE cells of the eye which was injected subretinally. At three hours after the injection, the RPE cells at the site of retinal tear had phagocytized more latex particles in their cytoplasm than RPE cells in normal retina. It can be concluded that RPE cells at the site of retinal tear had higher phagocytic and digestive activity than did RPE cells in normal retina.

Acid Phosphatase↗
PubMed1999

Photophysical studies of A2-E, putative precursor of lipofuscin, in human retinal pigment epithelial cells.

With age, human retinal pigment epithelial cells accumulate lipofuscin that can absorb photons in the visible range leading to light-induced damage and impaired vision. A putative precursor of lipofuscin, 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E, 5E,7E- octatetraenyl]-1-(2-hydroxyethyl)-4-[4-methyl-6-(2,6,6-trimethyl-1 - cyclohexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2-E), has recently been isolated and characterized from aged human retinal pigment epithelial cells. We have found that A2-E inhibits the growth of human retinal pigment epithelial cells at concentrations greater than 1 microM. Time-resolved fluorescence measurements of 1 microM A2-E in solution, performed under 413 nm excitation, showed that fluorescence wave forms integrated across the spectrum (450-600 nm) were best-fitted with three decay times in the nanosecond and subnanosecond time scale: 6.6, 1.9 and 0.33 ns. Untreated retinal pigment epithelial cells were characterized by three fluorescence lifetimes: 6.3, 1.7 and 0.35 ns. In retinal pigment epithelial cells treated with 1 microM A2-E, the fluorescence decay was significantly faster, with the marked presence (approximately equal to 30%) of a fourth short lifetime (0.12 ns). These fluorescence decay times for A2-E bound to human retinal pigment epithelial cells are similar to those of lipofuscin granules isolated from aged human retinal pigment epithelial cells. This similarity supports the hypothesis that A2-E is a precursor of lipofuscin and suggests that A2-E may play a role in the overall light damage associated with age-related retinal diseases.

Aging↗
PubMed1990

Antitransferrin receptor immunotoxin inhibits proliferating human retinal pigment epithelial cells.

Cultured human retinal pigment epithelial cells were exposed to an immunotoxin composed of a monoclonal antibody, 454A12, directed against transferrin receptors conjugated to a toxin, recombinant ricin A chain. Exposure of proliferating human retinal pigment epithelial cells to the immunotoxin (0.1 to 10,000 ng/mL) caused a statistically significant (P less than .0001) decrease in the number of cells. This inhibitory effect was induced after an exposure to the immunotoxin as short as 5 minutes and was maximal after 24 hours of exposure. The diminution in cell number was dose dependent over the range from 0.1 to 100 ng/mL. Monoclonal antibody alone, recombinant ricin A chain alone, or an irrelevant immunotoxin, MOP21C monoclonal antibody-recombinant ricin A, did not diminish the number of cells. There was a marked decrease in DNA synthesis measured by nuclear tritiated thymidine incorporation that accompanied the immunotoxin-mediated decrease in cell number. Viable cells remaining after exposure to the immunotoxin (0.1 to 10,000 ng/mL) were morphologically abnormal; typically the cells had elongated spindle-shaped processes and had lost their normal cuboidal appearance. In contrast, cell number was not decreased in confluent human retinal pigment epithelial cells after treatment with maximal doses of immunotoxin. Morphologic changes similar to those seen in proliferating cells were observed in confluent cells exposed to more than 100 ng/mL of immunotoxin. The effect of the immunotoxin was species specific because large doses of immunotoxin did not reduce the number of viable cells in proliferating or confluent pig retinal pigment epithelial cells or cause observable morphologic changes in this cell type. Our results indicate that the immunotoxin selectively inhibited proliferating retinal pigment epithelial cells by receptor-mediated internalization of the antitransferrin receptor monoclonal antibody-recombinant ricin A chain conjugate.

Cell Count↗
PubMed1991

Dispersion of retinal pigment epithelial cells from experimental retinal holes.

The effects of cryotherapy, transcleral massage, or directed irrigation on exposed retinal pigment epithelial (RPE) cells at the base of an experimental retinal hole were studied in living rabbit eyes. Cryotherapy or massage with or without vitrectomy failed to release RPE cells or result in preretinal membrane formation. Directed irrigation dispersed viable RPE cells into the vitreous and produced cellular precipitates with membranes on the inferior retina, although the membranes tended to regress within 6 weeks after surgery. These results suggest that healthy RPE cells at the base of retinal tears are not easily released into the vitreous and may not contribute to the formation of preretinal membranes found in proliferative vitreoretinopathy.

Animals↗
PubMed2001

Effects of the actin-stabilizing drug, jasplakinolide, on pigment granule motility in isolated retinal pigment epithelial (RPE) cells of green sunfish, Lepomis cyanellus.

The retinal pigment epithelium (RPE) of teleosts contains pigment granules that migrate in response to changes in light condition. Dissociated, cultured RPE cells in vitro can be triggered to aggregate or disperse pigment granules by the application of cAMP or dopamine, respectively. Previous research using the actin-disrupting drug, cytochalasin D, suggested that pigment granule motility is actin dependent. To further examine the role of actin in pigment granule motility, we tested the effects of the actin-stabilizing drug, jasplakinolide, on pigment granule motility. Pigment granules in previously dispersed RPE cells remained dispersed after jasplakinolide exposure (0.1-1 microM), but the drug halted movement of most pigment granules and stimulated rapid bi-directional movements in a small subset of granules. Jasplakinolide also blocked net pigment granule aggregation and interfered with the maintenance of full aggregation. Although jasplakinolide did not block pigment granule dispersion, it did alter the motility of dispersing granules compared to control cells; rather than the normal saltatory, primarily centrifugal movements, granules of jasplakinolide-treated cells demonstrated slow, creeping centrifugal movements and more rapid bi-directional movements. Jasplakinolide also altered cell morphology; the length and thickness of apical projections increased, and enlarged, paddle-like structures, which contained F-actin appeared at the tips of projections. Actin antibody labeling of jasplakinolide-treated cells revealed a more reticulated network of actin compared to antibody-labeled control cells. These results indicate that jasplakinolide-induced disruption of the actin network compromises normal pigment granule dispersion and aggregation in isolated RPE cells, thus providing further evidence that these movements are actin dependent.

Actins↗
PubMed2005

Toxicity of indocyanine green (ICG) in combination with light on retinal pigment epithelial cells and neurosensory retinal cells.

PURPOSE: To evaluate the toxicity of indocyanine green (ICG) in combination with light. METHODS: Human retinal pigment epithelial cells (ARPE-19) and rat neurosensory retinal cells (R28) were treated with four different concentrations of ICG in combination with light exposure. Cell viability, mitochondrial function, and DNA synthesis were measured. RESULTS: All concentrations of ICG with 10 min of light exposure caused a significant decrease in mitochondrial dehydrogenase activity in R28 and ARPE-19 cells. ICG without light exposure did not decrease mitochondrial dehydrogenase activity. In both cell lines, [(3)H]thymidine incorporation was increased when treated with ICG with or without light. R28 cells did not show any significant decrease in cell viability. CONCLUSIONS: The duration of light was a significant factor in ICG toxicity. ICG needs to be used with caution as it decreases the mitochondrial dehydrogenase activity and increases the DNA synthesis in retinal cells, markers for cell toxicity and dysfunction.

Animals↗