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PubMed2002

P-glycoprotein expression in human retinal pigment epithelium.

PURPOSE: The retinal pigment epithelium (RPE) is a transporting epithelial monolayer that controls hydration and composition of the subretinal space. P-glycoprotein is an ATP-binding cassette transport protein known to transport a wide range of hydrophobic compounds. The expression of P-glycoprotein in barrier epithelial cells suggests that it could serve a normal protective function, possibly clearing potentially harmful substances from sensitive compartments, like the subretinal space. The present study is designed to determine the expression and activity of P-glycoprotein in normal human RPE. METHODS: RT-PCR and direct sequencing were employed to examine the presence of mdr1 mRNA in cultured human RPE. P-glycoprotein-specific antibodies were employed in Western blotting to identify P-glycoprotein in cultured human RPE and in an established RPE cell line (D407). Anti-P-glycoprotein antibodies were also used to localize the protein in frozen, formaldehyde-fixed sections of native human RPE/choroid by immunohistochemistry. Finally, rhodamine uptake was performed in cultured human RPE monolayers to assess P-glycoprotein activity. The inhibitory antibody 4E3 and reversins 121 and 205 were used to block transport activity. RESULTS: P-glycoprotein is expressed, and is active, in human RPE tissue not exposed to any known inducers of P-glycoprotein. RT-PCR yielded a 546 bp product that was 100% identical in sequence to published data for the mdr1 isoform of human P-glycoprotein. Western blotting demonstrated expression at the protein level, with specific bands observed at about 220 and 165 kD. In native tissue, P-glycoprotein immunoreactivity was predominantly membrane associated, with localization to both apical and basolateral cell membranes. Finally, P-glycoprotein expressed in human RPE is active. Steady-state rhodamine accumulation was increased in the presence of compounds reported to block P-glycoprotein mediated rhodamine efflux. CONCLUSIONS: Human RPE, not exposed to inducer treatment, expresses P-glycoprotein with localization to both apical and basal cell surfaces. Basolateral P-glycoprotein could serve a protective function for the neural retina helping to clear unwanted substances from subretinal space. The finding that P-glycoprotein is also on the apical surface suggests possible additional roles for P-glycoprotein in the RPE.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2003

Effect of quiescence on integrin alpha5beta1 expression in human retinal pigment epithelium.

PURPOSE: The retinal pigment epithelium (RPE) is differentiated and mitotically inactive in the normal eye, but several pathologies such as proliferative vitreoretinopathy (PVR) cause RPE cells to dedifferentiate and resume proliferation. Integrins, a family of cell surface glycoproteins that mediate cell proliferation and differentiation, are thought to play fundamental roles in PVR. The aim of this study was to evaluate protein expression and gene regulation of the integrin alpha5 subunit in proliferating and quiescent RPE cells. METHODS: Protein expression was studied in situ by immunohistochemistry and in vitro at different cell confluences by immunoprecipitation. Semi-quantitative RT-PCR and transient transfections were used to determine whether increasing cell confluence also affected alpha5 subunit mRNA levels and promoter activity, respectively. RESULTS: We demonstrated that the integrin alpha5 subunit is present at the RPE cell surface both in situ and in vitro, and that alpha5 protein level is influenced by confluence. Levels of integrin alpha5 transcripts are similar for sub-confluent and confluent cells, and a small increase in the promoter activity was observed between sub-confluent and confluent cells. However, both the integrin alpha5 subunit transcript and the alpha5 promoter activity decreased when cells reached post-confluence. CONCLUSIONS: We demonstrated that cell confluence affected protein and gene expression of the integrin alpha5 subunit. Proliferating RPE cells expressed high levels of both the alpha5 protein and mRNA transcripts and showed a high promoter activity. However, when cells reached quiescence, alpha5 gene expression was substantially reduced and RPE cells expressed little alpha5 protein at their cell surface.

Adolescent↗

PubMed2005

Inhibition of vascular endothelial growth factor gene expression by T7-siRNAs in cultured human retinal pigment epithelial cells.

BACKGROUND: Retinal pigment epithelial (RPE) cells play an important role in the occurrence of choroidal neovascularization (CNV). Vascular endothelial growth factor (VEGF) as a positive regulatory growth factor is produced by the RPE in an autocrine or paracrine manner, promoting CNV development. Duplexes of 21 nt RNAs, known as short interfering RNAs (siRNAs), efficiently inhibit gene expression by RNA interference when introduced into mammalian cells. We searched for an efficient siRNA to interfere with VEGF expression in RPE cells and shed light on the treatment of CNV. METHODS: Human primary RPE (hRPE) cells were cultured and identified. Three pairs of siRNAs were designed according to the sequence of VEGF 1-5 extrons and synthesized by T7 RNA polymerase transcription in vitro. To evaluate the inhibitory activity of T7-siRNAs, hRPE cells were transfected via siPORT Amine. The interfering effect of T7-siRNAs in hRPE cells was examined by semiquantitative reverse transcription-polymerase chain reaction and immunofluorescence. RESULTS: Three pairs of T7-siRNAs synthesized by in vitro transcription with T7 RNA polymerase suppressed VEGF gene expression with efficiency from 65% to 90%. T7-siRNA (B), targeted region at 207 nt to 228 nt and double stranded for 21 nt with 2 nt UU 3' overhangs, was the most effective sequence tested for inhibition of VEGF expression in hRPE cells. Compared with nontransfected cells, the mean fluorescence in hRPE cells transfected with T7-sRNAs was significantly less (P < 0.01). siRNA with a single-base mismatch and ssRNA(+) did not show suppressing effect. Furthermore, it was found that siRNAs had a dose dependent inhibitory effect (5 to 10 pmol). CONCLUSION: T7-siRNA can effectively and specifically suppress VEGF expression in hRPE cells and may be a new way to treat CNV.

Base Sequence↗

PubMed1989

Topical phenylephrine for mydriasis affects rabbit retinal pigment epithelial transport.

Rabbit retinal pigment epithelium (RPE) has an alpha-1 adrenoreceptor that substantially reduces RPE short circuit current (Isc) when stimulated. Since phenylephrine is a potent alpha adrenergic agonist frequently used to obtain pupil dilation, we examined the effect of topically applied phenylephrine for pupil dilation on RPE transport. Naive black dutch-belted rabbits received either one drop of 10% phenylephrine applied at t = 0 and t = 30 min or one drop of 1% cyclopentolate applied at t = 30 min. At t = 50 min, RPE-choroid-sclera explants from these animals were sealed in an Ussing chamber. At t = 60-70 min, 1.4 X 10(-4) M epinephrine was introduced into both sides of the Ussing chamber. The change in Isc produced by epinephrine was measured. The Isc reduction in rabbits receiving phenylephrine was 26% (+/- 5% SD, n = 6). The Isc reduction in rabbits receiving cyclopentolate was 39% (+/- 6% SD, n = 5). These values are significantly different (P less than 0.02, student two-tail t-test). These results indicate that topical phenylephrine reached the RPE in vivo and prestimulated the alpha-1 adrenoreceptors.

Administration, Topical↗

PubMed1988

Mannose 6-phosphate receptors on the plasma membrane on rat retinal pigment epithelial cells.

The retinal pigment epithelium (RPE) phagocytizes the tips of photoreceptor outer segments (OS) during normal eye function. It is not known what ligand on OS is recognized by the RPE for removal from the interphotoreceptor matrix. It is possible that a sugar residue on a cell surface glycoconjugate of either the OS or RPE mediates the phagocytic interaction. Pinocytic experiments with a soluble mannose 6-phosphate ligand (125I-labelled mannosidase) showed that similar quantities of ligand were bound by RPE explants from Long Evans rat retinas and from Royal College of Surgeons (RCS/p+) rat retinas known to be defective in the phagocytosis of OS. The addition of mannose 6-phosphate reduced the total counts of bound alpha-mannosidase by 23% in both normal and dystrophic RPE explants. Mannose 6-phosphate receptors were visualized on normal and dystrophic RPE plasma membranes by immunocytochemical techniques. Further, phagocytosis was studied using phosphomannan-coated beads as phagocytic particles. Dystrophic RPE phagocytized phosphomannan-coated beads by a mannose 6-phosphate specific mechanism as shown by a significant reduction in the number of these coated beads taken up in the presence of the competing sugar. In contrast, normal RPE showed no uptake of phosphomannan-coated beads. Our findings indicate that a mannose 6-phosphate receptor is on the apical plasma membrane of rat RPE. This receptor may not be involved in normal OS phagocytic recognition, but may function in the trafficking of lysosomal enzymes by RPE cells.

Animals↗

PubMedDate not supplied

Characterization of laser-induced fluorescence in the canine retinal pigment epithelium.

The adult retinal pigment epithelium (RPE) exhibits fluorescence caused by various cytoplasmic flurophors and by lipofuscin. Microscopic investigations of fluorescence generally utilize continuum excitation sources (xenon, mercury) and varying filter combinations. Consequently, discrepant emission characteristics are often encountered in the literature. In the present study, an epi-fluorescence microscope linked to a laser source with defined excitation characteristics was used to examine fluorescence in normal, adult canine RPE. Excitation at 337 nm produced maximal fluorescence at 450 nm (blue), while excitation at 439 nm induced 550 nm (yellow) fluorescence. Continuous exposure of cells to 439 nm light caused an initial rapid reduction of intensity, with a subsequent slower decrease of the signal. After solvent extraction, fluorescence at 600 and 650 nm showed no major alterations relative to the values recorded at 550 nm. Our findings demonstrate that varying excitation wavelengths produce discrepant fluorescence data from RPE cells and indicate caution in direct comparisons between experiments where different excitation sources and filter combinations are used.

Animals↗

PubMed1983

Myeloid bodies in the mammalian retinal pigment epithelium.

In the retinal pigment epithelium (RPE) of a mammal, the Eastern gray squirrel, a type of cytoplasmic organelle, the so-called "myeloid body" that was previously thought to be restricted to the RPE of lower vertebrates was observed. In the squirrel, these organelles are continuous with the smooth endoplasmic reticulum (SER), lack an enclosing membrane, and in general exhibit all the morphologic criteria used to identify myeloid bodies. The presumptive myeloid bodies in the squirrel RPE are most prevalent in animals killed during the early hours of the dark period of a 12L:12D lighting cycle. They are rarely observed in animals killed just prior to or during the light period. Thus, these findings document for the first time the occurrence of myeloid bodies in the mammalian RPE, and indicate that their presence is influenced by a diurnal lighting cycle.

Animals↗

PubMed1994

Effect of TGF-beta on interferon-gamma-induced HLA-DR expression in human retinal pigment epithelial cells.

PURPOSE: Retinal pigment epithelial (RPE) cells express human leukocyte antigen (HLA)-DR (class II) antigens when stimulated with interferon gamma (IFN-gamma) and may be capable of local antigen presentation. The authors examined the effect of transforming growth factor-beta (TGF-beta), a cytokine normally found in the eye, on the expression of these immunoregulatory molecules in vitro and attempted to determine the mechanism by which this cytokine acts. METHODS: Human RPE cells were cultured in the presence of IFN-gamma and then stained immunohistochemically for HLA-DR antigens. TGF-beta 1 or TGF-beta 2 was added simultaneously with IFN-gamma or after 3 days of IFN-gamma treatment. In parallel experiments, RPE cells were pretreated with 4-phorbol-12 myristate-13 acetate (PMA), staurosporine, or calphostin C before stimulation with IFN-gamma or TGF-beta. Quantitative analysis was performed by fluorescence-activated cell sorting. RESULTS: IFN-gamma induced HLA-DR expression on RPE cells. Both TGF-beta 1 and TGF-beta 2 were able to inhibit this effect. These inhibitory effects of TGF-beta were augmented by pretreatment with either PMA or calphostin C. Pretreatment of the cells with PMA before stimulation with IFN-gamma downregulated HLA-DR expression. Staurosporine pretreatment suppressed HLA-DR expression by IFN-gamma-stimulated RPE cells, but this was not additive with TGF-beta. CONCLUSIONS: The authors conclude that TGF-beta 1 and TGF-beta 2 strongly inhibit the IFN-gamma-induced upregulation of class II antigens on human RPE cells. The modulation of these IFN-gamma and TGF-beta effects by calphostin C, staurosporine, and PMA treatment suggests involvement of the protein kinase C pathway.

Cells, Cultured↗

PubMed1998

A novel member of the Ig superfamily, RPE7, expressed on the retinal pigment epithelial cell and Müller cell of the bovine retina.

The retinal pigment epithelium of the vertebrate eye plays a major part in the maintenance of ocular function. To identify molecules involved in the exertion of their physiological functions, monoclonal antibodies against bovine retinal pigment epithelial cells were made. Analysis by immunofluoresence and immunoelectron microscopy showed that one of the monoclonal antibodies named anti-RPE7 stained the cell surface of retinal pigment epithelial cells and Müller cells. The anti-RPE7 antibody was revealed to recognize molecules of 45-55 kDa by Western blot analysis. Molecular cloning of the RPE7 cDNA and sequence analysis of the amino acids revealed that protein RPE7 belonged to the Ig superfamily. The high homology of RPE7 with metalloproteinase inducer suggests that the protein RPE7 might play a role in the matrix (interphotoreceptor matrix and basement membranes) remodeling as well as in retinal pigment epithelial cell migration under pathological conditions.

Amino Acid Sequence↗

PubMed1993

Visualization of [3H]docosahexaenoic acid trafficking through photoreceptors and retinal pigment epithelium by electron microscopic autoradiography.

PURPOSE: [3H]docosahexaenoic (DHA) acid was followed through the retinal pigment epithelial cells and photoreceptors for up to 5 days after injection to specifically determine which membrane systems of the retinal pigment epithelial cells are used in the handling of [3H]DHA after shedding and phagocytosis of rod tips. METHODS: Frogs (Rana pipiens) were injected with [3H]DHA in the dorsal lymph sacs, and maintained for up to 5 days. Retinas were processed for electron microscopic autoradiography, stored for various periods of time, and then analyzed by transmission electron microscopy. RESULTS: After 1 day, [3H]DHA had accumulated within photoreceptor ellipsoids, and had begun to appear as dense label in newly formed discs. By day 5, the basal region of dense label had expanded apically. Newly shed rod outer segment tips were diffusely labeled; but occasionally after several hours, they acquired additional label as they moved near Bruch's membrane. Retinal pigment epithelial cytoplasm maintained a constant level of label, with myeloid bodies sometimes slightly labeled. Oil droplets of the retinal pigment epithelium accumulated dense label throughout this study. CONCLUSIONS: When [3H]DHA enters the retinal pigment epithelium, some is retained within oil droplets, whereas the rest is passed on to the photoreceptors. [3H]DHA is initially taken up by inner segments and then dispersed to photoreceptor synaptic terminals as well as to ellipsoids where discs are assembled. Phagosomal labeling exactly matches rod outer segment tips, but occasionally increases as degradation occurs near Bruch's membrane. Normally, density of label remains constant throughout the degradation process.

Animals↗

PubMed1986

A retina-derived stimulator(s) of retinal pigment epithelial cell and astrocyte proliferation.

Retinal detachments are frequently accompanied by retinal pigment epithelial cell and glial cell proliferation. This may be important in the pathogenesis of proliferative vitreoretinopathy and may also play a role in the failure of some eyes to regain visual function despite anatomically successful retinal reattachment surgery. In this study, we demonstrate that a retina-derived substance or substances stimulates the proliferation of retinal pigment epithelial cells (250% above control) and astrocytes (150% above control) in vitro. The stimulation of proliferation occurs in the absence of serum, but is accentuated by serum. There is some degree of target-cell specificity as there is no stimulation of smooth-muscle-cell proliferation. Morphologic changes induced in the proliferating cell types as well as preliminary characterization suggest that one or more of the previously described eye-derived growth factors may be involved.

Animals↗

PubMed2006

Trafficking of osteonectin by retinal pigment epithelial cells: evidence for basolateral secretion.

Osteonectin is a glycoprotein that modulates several aspects of cellular behaviour including proliferation and adhesion. The retinal pigment epithelium forms a continuous monolayer of polarised cells immediately bellow the neuroretina, and is integral to the homeostasis of photoreceptor cells. While osteonectin is expressed by normal retinal pigment epithelium in situ, its expression is significantly increased in retinal pigment epithelial cells associated with several common retinal diseases. This pattern of expression implies an important role for osteonectin in the biology of retinal pigment epithelial cells. However, the trafficking, processing, and eventual fate of osteonectin in these cells is not clear at present. Although the theoretical report of a leader sequence within the osteonectin open reading frame and its extracellular presence in some tissues indirectly support secretion of the protein, there is no direct experimental demonstration of the secretion route to date. As a first step towards understanding the role of osteonectin in retinal pigment epithelium, we studied the intracellular distribution and trafficking of the protein in living cells. Here, we present experimental evidence that a precursor osteonectin fusion protein is targeted to the endoplasmic reticulum/Golgi pathway, with a likely basal secretion in retinal pigment epithelial cells. In addition, we show that the precursor osteonectin protein having the leader sequence masked fails to undergo secretion leading to cell death, a phenotype which may be of relevance not only for retinal pathology, but also for other diseases such as the bone disorder known as pseudoachondroplasia that is associated with a lack of osteonectin secretion.

Achondroplasia↗

PubMed2000

Controlled production of active cathepsin D in retinal pigment epithelial cells following adenovirus-mediated gene delivery.

The transduction of a low cathepsin D-producing retinal pigment epithelial cell line with a recombinant adenovirus, Ad.proCatD, carrying a viral promoter and the precursor form of the lysosomal enzyme cathepsin D, procathepsin D, led to the upregulation of proCatD expression. However, the resultant aspartic protease activity did not exceed that observed in normal primary human retinal pigment epithelial cells. Following the injection of Ad. proCatD into rat eyes, immunohistochemistry and Western blot analysis localized the expression of procathepsin D to the retinal pigment epithelial cell layer and to the sclera/choroid/retinal epithelial cell layers, respectively. This upregulation of procathepsin D expression was accompanied by a limited increase in aspartic protease activity. The injected eyes did not demonstrate any of the retinal changes that have been associated with the overproduction and secretion of active cathepsin D. Immunoelectronmicroscopy of Ad.proCatD-transduced retinal pigment epithelial cells demonstrated the presence of cathepsin D not only in cytoplasmic vesicles and lysosomes but also in the nucleoli and, less strongly, elsewhere in euchromatic regions of some 10% of cells. In spite of the upregulated expression of procathepsin D, the production of active cathepsin D in Ad.proCatD-transduced retinal pigment epithelial cells was strictly controlled. It is proposed that active cathepsin D production is controlled at the point of posttranslational modification by an intranuclear feedback mechanism initiated by the relative excess of procathepsin D in Ad. proCatD-transduced retinal pigment epithelial cells.

Adenoviridae↗

PubMed1988

Progressive ultrastructural damage and thickening of the basement membrane of the retinal pigment epithelium in spontaneously diabetic BB rats.

Ultrastructural examination of the neural retina and retinal pigment epithelium was performed in spontaneously diabetic BB rats and non-diabetic littermate controls at various time points during the course of diabetes. Four types of progressive changes occur in diabetic rats: (1) There is a progressive thickening of the basal laminae of the retinal pigment epithelium and the retinal capillaries. (2) In addition to this thickening, there is a progressive, often focal, thickening of the rest of Bruch's membrane, and by 11 1/2 months it contains numerous randomly oriented collagen fibrils. (3) There are progressive ultrastructural changes in retinal pigment epithelial cells consisting of marked dilation of the basal infoldings, the formation of large vacuoles and cell swelling. (4) Rare degenerative changes were noted in retinal capillary pericytes. Since non-diabetic littermates do not show comparable changes, it is likely that they are diabetes-related, suggesting that progressive damage to the retinal pigment epithelium may occur during the course of diabetes.

Aging↗

PubMed1994

Role of retinal pigment epithelium in the development of experimental autoimmune uveitis.

PURPOSE: To determine the role of retinal pigment epithelium in the induction of S-antigen-induced uveitis by administration of sodium iodate (NaIO3) to selectively damage the retinal pigment epithelium. METHODS: Forty-four Lewis rats were injected with 60 micrograms of S antigen in complete Freund's adjuvant. On postimmunization day 9 the rats were separated into four groups: three groups received NaIO3 at doses of 50, 25, and 10 mg/kg body weight, respectively, and the fourth group (control) received diluent. In addition, separate groups of animals (three in each group) received various doses of NaIO3 or diluent. All of the animals were killed on day 6 after NaIO3 injection, and the eyes were enucleated and submitted for light and electron microscopic examination. In addition, two groups of Lewis rats (6 in each group) were immunized with 0.5 ml of guinea pig spinal cord homogenate in complete Freund's adjuvant to induce experimental allergic encephalomyelitis. On postimmunization day 7, one group received NaIO3 at a dose of 50 mg/kg body weight, whereas the other group received diluent. All animals were killed between days 12 and 14, and spinal cord sections were obtained for microscopic examination. RESULTS: In the control group immunized with S antigen, severe (2+ to 4+) uveoretinitis developed in 70% of the animals. In contrast, only 18% of the animals injected with NaIO3 at a dose of 50 mg/kg body weight exhibited disease, and this was a mild (1+) form. The groups injected with 25 mg/kg (1+ to 2+) and with 10 mg/kg (2+ to 3+) of NaIO3 showed a mild to moderate degree of uveoretinitis in 27% and 50% of the animals, respectively. In the remainder of the animals there was no evidence of uveoretinitis. All of the NaIO3-treated animals showed selective necrosis of the retinal pigment epithelium; this was extensive in the higher dose group and focal in the lower dose groups. In the experimental allergic encephalomyelitis model there was no significant difference in incidence or histologic appearance of demyelinating disease in NaIO3- vs diluent-treated groups. CONCLUSIONS: These results indicate that the retinal pigment epithelium may play a role in the initiation and perpetuation of uveitis after sensitization with S antigen. The effect of NaIO3 appears to be localized to the retinal pigment epithelium; it had no effect on immune reactive cells, as evidenced by the development of experimental allergic encephalomyelitis in animals treated with NaIO3.

Animals↗

PubMed1981

Photoreceptor outer segment and retinal pigment epithelium in vitamin E deficient rats. An electron microscopic and electron histochemical study.

The photoreceptor outer segments and retinal pigment epithelium of vitamin E deficient rats were examined by electron microscope using electron histochemical techniques. In rats fed a vitamin E deficient diet for more than 6 months starting 20 days after birth, the photoreceptor outer segment showed vesiculation of the discs near the apical portion of the retinal pigment epithelium. In the retinal pigment epithelium, secondary lysosomes were increased in number. Reaction products of acid phosphatase activity were located in secondary lysosomes in the retinal pigment epithelium and on the disc membranes of the photoreceptor outer segment. These alterations became more prominent with the duration of vitamin E deficiency. It was assumed that the disc degeneration of the photoreceptor outer segment might be due to enhanced activity of lysosomal enzymes in the retinal pigment epithelium and the effect of released lysomal enzymes on the photoreceptor outer segment.

Animals↗

PubMed2006

Congenital hypertrophy of the retinal pigment epithelium (CHRPE) in familial colorectal cancer.

BACKGROUND AND AIM: Congenital hypertrophy of the retinal pigment epithelium (CHRPE) is a pigmented fundus lesion associated with familial adenomatous polyposis (FAP). CHRPE prevalence has been reported to be increased in subjects with familial or sporadic non-polyposis colorectal cancer (CRC), suggesting that some individuals with non-polyposis CRC have an attenuated form of FAP. Other studies have not confirmed these clinical observations and have failed to identify mutations in the gene responsible for FAP, but the reason for the discrepancy in relation to CHRPE prevalence has not been resolved. We determined the prevalence of CHRPE in subjects without CRC (negative control cohort), subjects with FAP (positive control cohort), and subjects with familial non-polyposis CRC (test cohort). METHOD: A cohort study consisting of 37 negative control subjects, 9 positive control subjects with documented APC gene mutations, and 36 test subjects with familial non-polyposis CRC but no identified pathogenic APC gene mutation. The diagnosis of hereditary non-polyposis colon cancer was excluded in the test cohort by testing for microsatellite instability in tumour tissue. RESULTS: None of the 37 people in the negative control group had CHRPE. Five of nine (56%) patients with FAP had multiple CHRPE lesions. None of the 36 subjects in the test cohort had CHRPE lesions. CONCLUSIONS: Ophthalmoscopy may contribute to risk assessment in families with FAP but not in familial non-polyposis CRC. Care must be exercised when interpreting pigmented fundus lesions because 8-13% of subjects in each of the cohorts had pigmented retinal lesions that were not CHRPE. Bilateral lesions and lesions with a depigmented halo were the hallmarks of CHRPE associated with FAP.

Adenomatous Polyposis Coli↗

PubMed1991

[Morphology of live retinal pigment epithelial cells].

We attempted to observe, by means of fluorescein angiography, the retinal pigment epithelial cells in pigmented rabbits. Fluorescein angiography was performed in 31 pigmented rabbits, after intravenous injection of 14mg/kg fluorescein sodium. The angiograms were evaluated as prints and as negative film under a light microscope. Animals were sacrificed and submitted to studies by scanning electron microscopy and fluorescein light microscopy. On fluorescein angiograms, we observed mosaic pattern which consisted of numerous polygonal spots overlying choroidal vasculature. Each polygonal spot showed central hypofluorescent area surrounded by hyperfluorescent rim. They were seen in all the eyes except 4 lightly pigmented eyes. They seemed to correspond, in size, to each retinal pigment epithelial cell. This pattern appeared from the early choroidal phase on, to become more distinct 5 to 15 minutes after dye injection. A hexagonal pattern was regularly seen away from the medullary rays by 3 or more disc diameters. The pattern became larger in the periphery than in the posterior pole. These angiographic findings closely matched those of retinal pigment epithelial cells as seen by scanning electron microscopy and fluorescein light microscopy in sizes and shapes. The findings indicate that it is possible to identify retinal pigment epithelial cells in pigmented rabbits by conventional fluorescein angiography.

Animals↗