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PubMed1987

Regulatory aspects of the in vitro development of retinal Müller glial cells.

Utilizing immunochemical and biochemical methods we have examined the maturation of retinal Müller cells in vitro both in monolayer cultures of dissociated tissue as well as rotation-mediated suspension culture of reaggregated embryonic retina cells. We have manipulated heterotypic cell-cell interactions through the use of such cell surface probes as plant lectins and monoclonal antibodies. In this report we show that the succinylated derivative of Con-A is capable of blocking neuronal-glial interactions in reaggregation cultures resulting in neuronal-glial segregation and failure of glial maturation. Furthermore, we describe a new monoclonal antibody which also inhibits glial maturation in vitro. This antibody recognizes an antigen which is present on retinoblast cells in general early in development, but becomes gradually restricted to Müller cells and to a much lesser extent photoreceptor cells during tissue maturation. The results further substantiate the regulatory influence of heterotypic cell-cell interactions in the development of retinal Müller cells and establishes probes for the analysis of the molecular basis of this phenomenon.

Animals↗
PubMed1991

Traumatic retinal detachment.

Seventy-seven patients developed retinal breaks following an episode of ocular contusion, and 65 (84.4%) of these developed rhegmatogenous retinal detachment. Surgical treatment successfully restored or maintained retinal apposition in 74 (96.1%) of the eyes. Thirty-six (46.8%) eyes recovered visual acuity of 6/9 or better. Of the retinal breaks recognised dialysis at the ora serrata was observed in 49 eyes, of which 28 were situated at the lower temporal quadrant. Seventeen eyes had irregular breaks arising within necrotic retina at the site of scleral impact. Twenty-four (31.2%) patients had retinal break or retinal detachment diagnosed within 24 hours of injury and 49 (63.6%) within six weeks. Immediate retinal detachment was a feature of necrotic retinal breaks, while inferior oral dialyses led to a slow accumulation of subretinal fluid. Delayed diagnosis of retinal detachment was due either to opaque media or to failure to examine the retina after injury. Visual prognosis was good when retinal break or detachment were diagnosed within six weeks of injury. However, those patients who escaped initial retinal examination and were lost to follow-up had a less favourable visual outcome.

Adolescent↗
PubMed2006

Endothelial nitric oxide synthase is expressed in amacrine cells of developing human retinas.

PURPOSE: To examine the expression and cellular distribution pattern of endothelial nitric oxide synthase (eNOS) in the developing human retina and to compare its expression with that in rats. METHODS: Expression of eNOS was examined by immunohistochemistry in retinas of humans ranging from 8.5 to 28 weeks of gestation (WG) and of rats. RESULTS: In the developing human retina, eNOS expression was first detected in the proximal margin of the neuroblastic layer in the incipient fovea-surrounding area at 12 WG. At 17 to 28 WG, eNOS-immunoreactive cells were located in the innermost part of the inner nuclear layer and in the ganglion cell layer, expanding to both temporal and nasal retinas and the processes projecting into the inner plexiform layer. These eNOS-positive cells coexpressed syntaxin and glutamate decarboxylase, and are probably GABAergic amacrine cells. The onset of eNOS expression in developing amacrine cells, however, preceded the invasion of retinal vasculature, long before vascular function involving these cells can be expected, suggesting that eNOS has a role not only in vasoregulation but also in retinal development. From 20 WG on, eNOS was also detected in the photoreceptors adjacent to the fovea. eNOS expression in amacrine cells and photoreceptors was observed in the central-to-peripheral and temporal-to-nasal gradients. However, in the developing rat retina, eNOS was expressed exclusively in the vascular endothelial cells. CONCLUSIONS: The results support that eNOS plays a role, not only in the regulation of vascular function but also in the process of retinal development in humans.

Amacrine Cells↗
PubMed1992

Onset of retinopathy of prematurity as related to postnatal and postconceptional age.

The hypothesis that both perinatal events and stage of retinal development are important factors in determining the age at onset of retinopathy of prematurity (ROP) was tested by comparing gestational age at birth with postnatal and postconceptional age when ROP (using ICROP) was first seen. The study population consisted of 207 infants (111 placebo (P) treated, 96 vitamin E (E) treated) who developed ROP among a group of 914 premature infants (460 P, 454 E) enrolled in a randomised clinical trial of the effect of prophylactic use of vitamin E at pharmacological serum levels on incidence and severity of retinopathy. The mean postnatal age at onset of retinopathy was delayed in E treated infants compared with P treated infants by 1.4 weeks (t = 4.004, p < 0.0001). For both P and E treated infants postnatal age at onset of ROP (which reflects the state of retinal development at which birth insults occur) and postconceptional age at onset of ROP which defines state of maturity) were correlated with gestational age at birth. This suggests that both the event of premature birth and the extent of retinal development are important in determining when ROP will first be observed.

Aging↗
PubMed1988

Development of ganglion cell topography in ferret retina.

The adult ferret has approximately 90,000 retinal ganglion cells, arranged in a prominent area centralis and visual streak. The role of differential cell generation, cell death, and retinal growth in the control of adult retinal ganglion cell number and distribution was evaluated by examining basic aspects of retinogenesis, including growth in retinal area, developmental changes in the number, size, and distribution of retinal ganglion cells (identification aided by retrograde transport of HRP), and the incidence of degenerating cells in the ganglion cell layer. Retinal development in the ferret was also compared to retinal development in the cat (which has an even more differentiated area centralis) to determine what alterations of developmental parameters are most closely associated with this species difference in adult morphology. The area of the retina increases linearly from birth (12 mm2) to postnatal day 24 (54 mm2), reaching an eventual adult value of 64 mm2. Ganglion cell numbers peak at 155,000 (approximately twice the adult number) on postnatal day 3, and fall to adult numbers by postnatal day 6. The remaining cells of the ganglion cell layer, principally displaced amacrine cells, reach their peak number on postnatal day 10 (approximately 280,000), falling to 200,000 by adulthood. Degenerating cells are abundant in the ganglion cell layer in the immediate postnatal period. A difference in the incidence of degenerating cells in the presumptive area centralis versus that in the retinal periphery was not observed postnatally, though there were other striking spatial nonuniformities, suggesting that differential cell loss might contribute to other features of retinal topographic organization. Ganglion cell density is virtually uniform across the retina at birth. Cell density is first reduced in the dorsal retina, resulting in a dorsal-to-ventral gradient in cell density that persists until day 10, when ganglion cell number has stabilized. By postnatal day 24, an area centralis and visual streak has emerged, but not of adult magnitude. Because ganglion cell number has stabilized long before the area centralis and visual streak emerge, we conclude that differential retinal growth is the principal mechanism producing this feature of retinal topography. Comparison with the cat suggests that the proportionately greater nonuniform growth of the cat's eye accounts for the greater differentiation of its area centralis.

Algorithms↗
PubMed2006

Causes of visual acuity loss among patients with AIDS and cytomegalovirus retinitis in the era of highly active antiretroviral therapy.

PURPOSE: To quantitate the frequencies of the common causes of visual acuity loss for patients with AIDS and cytomegalovirus (CMV) retinitis in the era of highly active antiretroviral therapy (HAART). DESIGN: Multicenter prospective observational study. PARTICIPANTS: Three hundred seventy-nine patients (494 eyes) with CMV retinitis. METHODS: Follow-up every 3 months with medical history, ophthalmologic examination, and laboratory testing. MAIN OUTCOME MEASURES: Loss of visual acuity across the 20/50 or worse and 20/200 or worse thresholds and doubling of the visual angle; frequencies of causes of such vision loss. RESULTS: Overall, involvement of the posterior pole with CMV retinitis (zone 1 retinitis) accounted for approximately one half of incident visual acuity loss of 20/50 or worse, 20/200 or worse, and of doubling of the visual angle. Cataract and retinitis-related retinal detachment were the second and third most common causes of vision loss, accounting for 22% to 33% and 13% to 20% of vision loss for the 3 outcomes, respectively. In subset analysis, cataract and cystoid macular edema (CME) accounted for approximately 50% of incident vision loss in eyes of patients with longstanding CMV retinitis and immune recovery at baseline, but these complications accounted for <10% of incident vision loss in eyes of patients with newly diagnosed CMV retinitis at baseline. Of eyes that had a vision-threatening complication of CMV retinitis, eyes that developed retinal detachment had the highest risk of vision loss, with 100% of eyes developing visual impairment (20/50 or worse vision) and 42% of eyes developing legal blindness (20/200 or worse vision) at 12 months after diagnosis of the retinal detachment. CONCLUSIONS: In the HAART era, zone 1 involvement and retinal detachment remain the most common causes of visual acuity loss among patients with CMV retinitis. Cataract and CME also are common causes of loss of visual acuity, primarily in those patients with HAART-induced immune recovery.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Novel expression pattern of interphotoreceptor retinoid-binding protein (IRBP) in the adult and developing zebrafish retina and RPE.

PURPOSE: Interactions between the neural retina and retinal pigment epithelium (RPE) are mediated by the interphotoreceptor matrix (IPM). The transport of retinoids across the IPM is mediated by interphotoreceptor retinoid-binding protein (IRBP). To explore the possibility that IRBP is important during retinal development, we examined its spatiotemporal expression pattern in embryonic zebrafish. METHODS: IRBP mRNA expression was examined using RT-PCR and in situ hybridization. IRBP was localized using antiserum against recombinant zebrafish IRBP. IRBP synthesis and secretion were studied by in vitro metabolic labeling of retinas and RPE-eyecups. RESULTS: IRBP mRNA was first observed in the pineal at 24 hours post-fertilization (hpf) and in the ventral retina at 50 hpf. Immunoreactive IRBP was first observed at 72 hpf. Remarkably, IRBP was expressed not only by photoreceptors but also by the adult and embryonic RPE. In embryos, expression in both retina and RPE began in a ventronasal patch and spread to involve the entire eye. In general, early IRBP expression was dominated by photoreceptors, but then RPE expression spread beyond the limit of photoreceptor expression. Double in situ hybridizations suggests that cones express IRBP mRNA before they express a specific opsin, while rods may express rod opsin prior to IRBP. CONCLUSIONS: The temporal and spatial patterns of IRBP expression by the RPE and retina are consistent with a role in retinal development and suggest coordination of RPE and photoreceptor differentiation.

Animals↗
PubMed1988

Sodium channel expression and assembly during development of retinal ganglion cells.

Acquisition of functional Na+ channels is a critical event in the development of a neuron because it allows the generation of conducted action potentials. alpha subunit mRNA is first detected in developing rat retina at 1% of its maximum level on embryonic day 15, 4 days after the first ganglion cells are formed. alpha subunit protein is detected in the axons of the ganglion cells at this time, but beta 1 subunits, beta 2 subunits, and high affinity saxitoxin binding sites are not detected until after birth. There is an approximately coordinate increase in alpha subunit mRNA, alpha, beta 1, and beta 2 subunit protein, assembled complexes of alpha, beta 1, and beta 2 subunits, and high affinity saxitoxin binding sites between postnatal days 7 and 21. Expression of alpha subunit genes is an early event in ganglion cell differentiation, and both gene transcription and posttranslational assembly are separate, rate-limiting steps in development of Na+ channels.

Animals↗
PubMed2003

COX-2 inhibition and retinal angiogenesis in a mouse model of retinopathy of prematurity.

PURPOSE: The prostaglandin-cyclooxygenase (COX) pathway influences new blood vessel growth in a variety of tissues. This study was conducted to determine the cellular location of COX-2 in the retina and whether the inhibition of COX-2 would reduce retinal angiogenesis in a rodent model of retinopathy of prematurity (ROP). METHODS: ROP was induced in C57BL/6 mice by exposing 7-day-old mice to 75% oxygen (hyperoxia) for 5 days followed by 5 days in room air (relative hypoxia and retinal angiogenesis). Normal mice were those with a normally developing retinal vasculature exposed to room air from birth until postnatal day (P)17. The COX-2 inhibitor, rofecoxib (15 mg/kg body weight intraperitoneally) was administered to normal and ROP mice from P12 to P17. Immunohistochemistry for COX-2 was performed on retinas from all groups by the avidin-biotin method. Histologic methods were used to count blood vessel profiles (BVPs) in the inner retina (inner limiting membrane, ganglion cell layer, and inner plexiform layer) with a masked approach. RESULTS: Intense COX-2 immunolabeling was specifically localized to ganglion cells and blood vessels of all mice retinas. In ROP mice, COX-2 immunolabeling was detected on blood vessels extending into the vitreous cavity. Quantitation of BVPs in the inner retina revealed an increase in untreated ROP mice compared with untreated normal mice (P < 0.001). Rofecoxib decreased BVPs by approximately 45% in normal mice and 37% in ROP mice. CONCLUSIONS: COX-2 is localized to sites associated with retinal blood vessels. The finding that the selective COX-2 inhibitor, rofecoxib, attenuated the retinal angiogenesis that accompanies ROP, and normal retinal development indicates that COX-2 plays an important role in blood vessel formation in the retina.

Animals↗
PubMed1997

Involvement of AP-2 in regulation of the R-FABP gene in the developing chick retina.

Little is known regarding the molecular pathways that underlie the retinal maturation process. We are studying the regulation of the retinal fatty-acid-binding protein (R-FABP) gene, highly expressed in retinal precursor cells, to identify DNA regulatory elements and transcriptional factors involved in retinal development. Although the upstream sequence of the R-FABP gene is extremely GC rich, CpG methylation in this region is not implicated in the regulation of this gene because the 5' flanking DNA remains unmethylated with tissue differentiation when there is a dramatic decrease in R-FABP transcript levels. Using a combination of DNase I hypersensitivity experiments, gel shift assays, and DNase I footprinting, we have found three sites of DNA-protein interaction within 205 bp of 5' flanking DNA in the undifferentiated retina and four sites in the differentiated retina. DNA transfection analysis indicates that the first two footprints located within 150 bp of 5' flanking DNA are required for high levels of transcription in primary undifferentiated retinal cultures. The first footprint includes a putative TATA box and Spl binding sites while the second footprint contains a consensus AP-2 DNA binding site. Supershift experiments using antibodies to AP-2 and methylation interference experiments indicate that an AP-2-like transcription factor present in both late-proliferative-stage retina and differentiated retina binds to the upstream region of the R-FABP gene. A combination of data including the expression profile of AP-2 during retinal development and DNA transfection analysis using constructs mutated at critical residues within the AP-2 binding site suggests that AP-2 is a repressor of R-FABP transcription.

Animals↗
PubMed2005

Pupillary evaluation of retinal asymmetry: development and initial testing of a technique.

Glaucomatous damage to upper and lower retina is often unequal. We have developed a rapid, objective, quantitative measure of asymmetry of retinal sensitivity, using infrared pupillometry and pairs of large stimuli that are symmetric about the horizontal meridian. Results for a group of 11 young subjects free of eye disease indicate that the distribution of asymmetry is close to a normal distribution centered near upper/lower symmetry. Some subjects showed modest amounts of asymmetry, which was relatively uniform within each eye, and between the two eyes, of the subject. This approach to determination of asymmetry within an eye is potentially applicable to testing patients with glaucoma. The narrowness of the distribution should make it possible to detect asymmetries caused by disease.

Adult↗
PubMed1983

Development of retinal amacrine cells in the mouse embryo: evidence for two modes of formation.

Developing amacrine and ganglion cells have been graphically reconstructed from a series of 567 consecutive thin sections of the E17 mouse retina on the first day when an obvious inner plexiform layer (IPL) is present and 2 days later than for our previous study of amacrine cell formation at E15 (Hinds and Hinds ('78). At E17 amacrine cells of the neuroblastic layer (normally placed amacrine cells), unlike those at E15, appear to develop directly from ventricular cells; intermediate elements are bipolar-shaped cells with terminal arborization in the IPL. On the other hand, the development of displaced amacrine cells and some normally placed amacrine cells at E17 appears to closely resemble that described for all amacrine cells at E15: derivation from "ganglion cells" by loss of the axon and transformation of the cell. Three lines of evidence support this conclusion. (1) Cells have been found that resemble ganglion cells except that they have only an apparent axon remnant and have somata restricted to the IPL and the immediately adjacent portion of the ganglion cell layer (GCL); amacrine cells transitional between these cells and the smaller and darker, normally placed amacrine cells also occur in the IPL. (2) Axons of two ganglion cells have been found which appeared to be in the process of breaking up and degenerating. (3) The fraction of anaxonic cells with somata in the GCL (two out of 79, or 3%) or in the GCL plus IPL (ten out of 88 or 11%) is too small to account easily for the large fraction (probably at least 45%) of displaced amacrine cells found in the adult, even with conservative assumptions (P less than 0.05). A mathematical model suggests that approximately 40% of the ganglion cells present at E17 will lose their axon, and of these around half will migrate to the neuroblastic layer, while the other half will become displaced amacrine cells. The results suggest a natural explanation for the recent finding that wide field amacrine cells are found with somata on both sides of the IPL, while narrow field amacrine cells are never displaced: the former may be derived from ganglion cells by loss of the axon, while the latter may be formed directly from ventricular cells.

Animals↗
PubMed1999

Incidence and risk factors for developing cytomegalovirus retinitis in HIV-infected patients receiving protease inhibitor therapy. Spanish CMV-AIDS Study Group.

OBJECTIVE: To assess the incidence and risk factors for cytomegalovirus (CMV) retinitis in HIV-infected patients who initiated protease inhibitor-containing antiretroviral therapy. DESIGN AND SETTING: Prospective, multicentre study. PATIENTS: A cohort of 172 HIV-infected patients with a CD4 cell count below 100x10(6) cells/l at the time of protease inhibitor introduction. MAIN OUTCOME MEASURES: Confirmed CMV retinitis and mortality, according to CD4 cell count, HIV load, and CMV viraemia. RESULTS: The cumulative incidence of CMV retinitis was 5% at 1 year and 6% at 2 years. Only a positive CMV polymerase chain reaction (PCR) test at therapy initiation was significantly associated with the development of disease (relative hazard, 4.41; 95% confidence interval, 2.12-8.93; P<0.00001). The 12-month Kaplan-Meier CMV retinitis event rate was 38% in patients who were CMV PCR-positive compared with 2% in those who were CMV PCR-negative (P<0.001). Mean CMV load was significantly higher in those individuals who went on to develop CMV retinitis (3700 versus 384 copies/ml, P = 0.002). Only 2% of patients remained CMV PCR-positive after 3 months of protease inhibitor therapy, and CMV viraemia was not associated with a worse therapy response or shorter survival. Transient CMV positivity without a higher risk of disease was observed in 7% of patients at the first month on therapy. CONCLUSIONS: Protease inhibitor-containing antiretroviral therapy significantly reduces the incidence of CMV viraemia and disease. Although a positive CMV PCR test identifies those patients on therapy at highest risk of CMV retinitis, it is not associated with an increased risk of death or a worse response to protease inhibitor therapy.

AIDS-Related Opportunistic Infections↗
PubMed1975

Retinal detachment in retrolental fibroplasia.

Retrolental fibroplasia is a continuing problem in ophthalmology and may lead to retinal detachment. In this study, two groups of patients with retrolental fibroplasia and retinal detachment are described. The first group consists of youngsters who develop retinal detachment during their teenage years and frequently have not been diagnosed as having the disease until the retina detaches. Usually definite retinal breaks can be found near the equator and these are round or oval in appearance and without opercula. A second group of patients was noted to develop retinal detachment at an earlier age. The configuration of these detachments suggested a rhegmatogenous etiology, but retinal breaks were hard to detect because the peripheral retina was frequently obscured by a membrane or cataract. Additional evidence to support this opinion was provided when a small retinal hole was identified in one youngster whose ora could be easily seen. Because of the progressive nature of vitreoretinal adhesion in retrolental fibroplasia, it is advocated that youngsters with any evidence of retrolental fibroplasia at the time of discharge from the premature nursery be followed at one month, three months, and six months of age and at four-month intervals thereafter until the age of four years. If no difficulty develops by the time, yearly examinations suffice. Follow-up examinations are important because when prompt diagnosis of retinal detachment is made, the involved eye can often be salvaged with surgery.

Adolescent↗
PubMed1996

Mash1 promotes neuronal differentiation in the retina.

BACKGROUND: Mash1, a mammalian homologue of Drosophila achaete-scute proneural gene complex, plays an essential role in differentiation of subsets of peripheral neurones. Whereas Mash1 is expressed during retinal development, no apparent abnormalities were found during embryogenesis as well as at birth in Mash1-null retina, suggesting that early differentiating cells such as ganglion, amacrine and cone cells develop normally. Because Mash1-null mice die soon after birth, their postnatal development cannot be examined in vivo. Thus, it remains to be determined whether or not Mash1 functions in postnatal development of retina. RESULTS: Here, Mash1 roles in postnatal development of retina was examined by using retinal explant that develops like in vivo retina. Without Mash1, differentiation of late appearing cells such as rod, horizontal, and bipolar cells was delayed and the final number of bipolar cells was significantly reduced. In contrast, vimentin-positive cells (probably Muller glial cells) were increased in Mash1-null retina. CONCLUSIONS: These results provide evidence that Mash1 promotes neuronal differentiation during retinal development and is essential for proper ratios of retinal cell types.

Animals↗
PubMed1993

Diurnal growth rhythms in the chicken eye: relation to myopia development and retinal dopamine levels.

1. If the eyes of young chickens are deprived of clear vision by translucent occluders, they develop considerable amounts of axial myopia within days. At the same time, the day time retinal dopamine levels drop by about 30%. Because the retinal dopamine levels of normally sighted chicks also differ diurnally and are low at night, we expected that the rate of axial eye growth might also differ during this time. 2. Unexpectedly, eyes grew in length only during the day (about 0.13 mm/day) and even shrank during the night (about -0.04 mm/night, average net growth +0.09 mm in 24 h). 3. If the eyes were occluded, they grew both during the day and also at night (average net growth: +0.16 mm in 24 h). Therefore, development of deprivation myopia was a result of the lack of growth inhibition at night rather than of excessive growth during the day when the actual deprivation occurred. 4. Suppression of dopaminergic retinal pathways by intravitreal injections of the neurotoxin 6-hydroxy-dopamine (6-OHDA) also suppressed development of deprivation myopia and it restored the growth inhibition at night. With normal visual experience, the drug had no effect on axial eye growth and refractive state. 5. Diurnal growth rhythms of the eyes disappeared under continuous light.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The origin and development of retinal astrocytes in the mouse.

Astrocytes, a class of glia which appear in the mammalian retina late in development, have been postulated either to originate in situ from Müller cells or extra-retinally from the optic stalk epithelium, only subsequently invading the eye. The site of origin and the developmental characteristics of retinal astrocytes were examined in the mouse, a species not previously studied for this purpose. Sections of normal eyes and stalks at different ages were examined. Cells positive for glial fibrillary acidic protein (GFAP) were first observed at post-conceptional day 17 at the optic disc end of the stalk. From this site, the GFAP-positive cells migrated into and across the retina at a rate of approximately 290 microns per day, reaching its edge by post-conceptional day 28. While migrating across the retina, the astrocytes progressively increased in size and morphological complexity, observations confirmed by measurement of their fractal dimension. Over the same period, a wave of differentiation swept along the stalk in the cranial direction. Further evidence that retinal astrocytes are born outside the retina emerged when foetal hemiretinae with or without optic stalks were explanted to the chorioallantoic membrane of the chick. When examined one to twelve days later, no explant cultured without the optic stalk contained GFAP-positive astrocytes, while explants with the stalk left attached contained relatively normal numbers of astrocytes. We observed, using fluorescence confocal microscopy, that retinal astrocytes in the mouse as in the rat, associate predominantly with blood vessels, not axonal bundles. It was of interest to determine whether this class of glia is essential to the normal cytoarchitectural development of the neural retina. Morphological analysis of the explants revealed no observable differences in cytoarchitecture or in the timing of developmental events between retinae maturing with or without astrocytes. It was therefore concluded that astrocytes may not be essential to the normal structural development of the murine retina.

Allantois↗