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PubMed1990

Early expression of the gene for interphotoreceptor retinol-binding protein during photoreceptor differentiation suggests a critical role for the interphotoreceptor matrix in retinal development.

Interphotoreceptor retinol-binding protein (IRBP), the major protein component of the subretinal space, is in a strategic position to mediate cellular interactions between the retinal pigmented epithelium (RPE) and the neural retina. While IRBP appears to be involved in vitamin A transport during the visual cycle in the adult, the role of this protein during eye development has not been determined. As a first step to understanding the role of IRBP during retinal development, we have studied the expression of the mRNA for this glycolipoprotein during photoreceptor differentiation in the rat. A rat neural retina cDNA library was prepared from which an IRBP clone was isolated. The clone contains an open reading frame followed by a 3' noncoding sequence ending in 10 adenosine residues. The coding region has an identity of 83.9 and 82.5% with the nucleotide sequence of human and bovine IRBP, respectively. Rats (Sprague-Dawley, Wistar, and Royal College of Surgeon pink-eyed controls) have a 6.4 and a 5.2-kb mRNA for IRBP which are present in a 1:4 ratio and thus are the only vertebrate known to definitely have more than one major form of the IRBP message. Genomic Southern blots are consistent with the hypothesis that there is only one allele of the IRBP gene, suggesting that the two forms are produced by alternative processing of the mRNA. To generate an antisense RNA probe for use in molecular titration assays and Northern blots, an Eco RI-Bam HI fragment from the coding region was subcloned in between flanking Sp6 and T7 promoters. Total RNA was prepared from undissected rat globes from postnatal days p0-p22. The expression of the mRNA for IRBP was studied by Northern blots and the level of the transcripts determined by solution hybridization assays. Approximately 10(5) IRBP mRNA transcripts/micrograms total eye RNA are present at birth. This increases to a final level of 3.1 X 10(6) transcripts/micrograms total RNA by p9. The one-half maximal level of the mRNA occurs at p4.2 which is 2 wk before the one-half maximal level of IRBP is reached in the subretinal space (Gonzalez-Fernandez, F., R. A. Landers, P. A. Glazebrook, S.-L. Fong, G. I. Liou, D. M. K. Lam, and C. D. B. Bridges. 1984. J. Cell Biol. 99:2092-2098). The expression of the mRNA for IRBP reflects the developmental emergence of the interphotoreceptor matrix as an important structure within the retina.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1984

Use of a culture system to identify possible causes of abnormal retinal development.

The aim of this study was to apply a recently developed cell culture system to the problem of identifying possible etiologies of altered retinal maturation. Using techniques of electrophysiology and neuropharmacology, it was possible to monitor the release of acetylcholine at synapses formed by cultured retinal neurons derived from the fetal rat. The major finding of this study was that the functional development of cholinergic retinal neurons of the fetus could be altered if the mother rat had been injected with a synthetic glucocorticoid hormone or stressed by cold exposure during a critical period in pregnancy. Thus, the maturation of at least certain fetal retinal neurons appears to be influenced by factors affecting the mother. The culture system described here provides a potentially useful approach to the identification and investigation of possible causes of abnormalities in the functional development of the mammalian retina.

Animals↗
PubMed1999

Misexpression of cNSCL1 disrupts retinal development.

cNSCL1 is the chick homologue of mammalian NSCL1, a basic helix-loop-helix gene transiently expressed during neurogenesis. To gain insight into its function, we studied the involvement of cNSCL1 in retinal neurogenesis. In situ hybridization showed dynamic, cell-type-specific expression of cNSCL1, first in developing ganglion cells and later in glial cells. This is drastically different from the expression of neuroD in young photoreceptor cells and their precursors, demonstrating that the proposed neurogenin --> neuroD --> NSCL1 cascade might not apply to retinal neurogenesis in the chick. Small eyes were produced when cNSCL1 was misexpressed in the retinal neuroepithelium through viral transduction. Pulse-labeling with BrdU and [(3)H]thymidine revealed a significant decrease in cell proliferation activity with cNSCL1 misexpression. Massive cell death occurred, but only after cell proliferation activity had subsided, resulting in major distortions of retinal structure. Our data demonstrate the importance of regulated expression of cNSCL1 during retinal development.

Animals↗
PubMed2004

Effect of over-expression of pigment epithelium derived factor (PEDF) on developing retinal vasculature in the mouse.

PURPOSE: Pigment epithelium derived factor (PEDF) is a secreted protein with demonstrated anti-angiogenic properties, and with potential application for the treatment of neovascular disease. Delivery of pigment epithelium derived factor to the retina via virus mediated gene transfer has been shown to inhibit neovascularization in a number of experimental models. While pigment epithelium derived factor is endogenously expressed in the retina, its role in guiding normal vessel development and growth is not yet known. This study aimed to determine whether over-expression of pigment epithelium derived factor alters the normal pattern of retinal vessel development. METHODS: Neonatal (age postnatal day 2 (P2)) CD1 mice were injected subretinally unilaterally with AAV2/1.CMV.PEDF while contralateral eyes were injected subretinally with AAV2/1.CMV.EGFP as control. Cohorts of animals were sacrificed at P7 to P21 and the retinal vasculature was co-labeled through fluorescein-dextran perfusion and immunohistochemistry. Vascular size, localization, and structure were analyzed using light and confocal microscopy. Additional cohorts were use to obtain quantitative levels of pigment epithelium derived factor protein through ELISA. RESULTS: The extent of vessel growth from the optic disk to periphery over time (i.e., the radius of retinal vasculature), and the area of expansion of the neural retina were unaffected by over-expression of pigment epithelium derived factor to levels at least 3.5 fold higher than endogenous levels. The thicknesses of the various retinal layers were similar in AAV2/1.CMV.PEDF treated and control injected eyes. Three dimensional analysis of confocal images shows a slight delay in the rate of growth of vasculature into the deeper layers of the retina in pigment epithelium derived factor treated eyes compared to EGFP treated control eyes. However, the normal differentiation of vessels into arterioles, and venules, and the formation of a capillary network continued to occur, achieving normal and complete maturation of vascular structure by P21. CONCLUSIONS: Over-expression of pigment epithelium derived factor in the developing retina exerted no marked or permanent effects on retinal vessel growth and differentiation. The findings are relevant to the safety of the potential therapeutic use of pigment epithelium derived factor in human retinal disease.

Animals↗
PubMed2004

MyoD-lacZ transgenes are early markers in the neural retina, but MyoD function appears to be inhibited in the developing retinal cells.

Recent findings suggest that eye and skeletal muscle development in vertebrates share the same regulatory network. In that network, Pax3 gene is apparently activated through Dach/Eya/Six feedback loop to mediate MyoD-driven myogenesis. The purpose of this study was to investigate previously reported MyoD-lacZ expression in the developing mouse neural retina and to gain insight into the potential role of MyoD in the embryonic retinal cells. The analysis of MD6.0-lacZ and 258/-2.5lacZ transgenic embryos revealed that the retinal temporal expression pattern of the two transgenes resembled their expression pattern in the MyoD-dependent precursor muscle cells. However, MyoD transcripts and protein could not be found in the sites of MyoD-lacZ retinal expression. Furthermore, our immunohistochemical analysis suggests the existence of diverse factors (e.g., Pax6 and Chx10) within the retinal cells that differentially and inappropriately activate the two transgenes. Finally, the retinal phenotype observed in Pax7-/- knock-out mice suggests a role for Pax7 in photoreceptor cell differentiation, retinal lamination and in the etiopathology of retinoblastoma. Taken together, our data suggest that the MyoD gene evolved a different mechanism to achieve its down-regulation within the retina than that of the Myf5 gene.

Animals↗
PubMed2003

Regulation of ganglion cell production by Notch signaling during retinal development.

Although progenitor cells in developing vertebrate retina are capable of producing all retinal cell types, they are competent to produce only certain cell types at a given time, and this competence changes as development progresses. We asked whether a change in progenitor cell competence is primarily responsible for ending production of a specific cell type, the retinal ganglion cell. Reducing Notch expression using an antisense oligonucleotide in vitro or in vivo increased ganglion cell genesis. The antisense treatment could reinitiate ganglion cell genesis after it had terminated in a region of the retina, but only for a brief period. The failure of the Notch antisense treatment to reinitiate ganglion cell production after this period was not due to the lack of receptor or ligand expression, as both Notch-1 and Delta-1 were still expressed. The failure of the Notch antisense treatment to reinitiate ganglion cell production is consistent with the suggestion that the intrinsic competence of progenitor cells changes as development progresses. Because reducing Notch signaling can reinitiate ganglion cell production for a brief period after ganglion cell production has normally ceased, it appears that ganglion cell production initially ends in a region of the retina because of cell-cell interactions and not because progenitor cells lose the competence to make ganglion cells. Notch signaling appears to temporarily prevent production of ganglion cells in a region, while some other signal must initiate a change in progenitor cell competence, thus permanently ending the possibility of further ganglion cell production.

Animals↗
PubMed1989

Morphological findings during retinal development and maturation in hereditary rod-cone degeneration in Abyssinian cats.

The sequence of structural changes involved in postnatal photoreceptor differentiation, maturation and early degeneration was studied in young Abyssinian cats and kittens with hereditary rod-cone degeneration and compared to maturation in normal controls. In affected cats the earliest change seen was disorientation of outer segment discs in the majority of the rods, while other rods appeared to develop and mature normally. Such disorientation of discs (at oblique angles or parallel to the longitudinal axis of the outer segment, or whorls of discs) is considered as 'immaturity', since controls also showed a substantial number of disoriented rod outer segment discs at this young age. At postnatal day 35 the difference between affected animals and controls was marked with a high frequency of immature appearing rod outer segment discs in affected animals, while all rod outer segment discs were adult-like and arranged in an orderly manner in controls. Cones seemed unaffected at this age. More severe changes in affected rod outer segments in the form of disintegration of discs (vacuolization and clumping of disc material, or formation of debris), which we consider to represent degeneration, were first observed at the time when retinal maturation normally occurs in the cat, i.e. 150 days postnatally. Subsequently a drop-out of rods was seen, primarily of rods with disoriented and disintegrated outer segment discs, followed by a slow, progressive degeneration of rods that had developed and matured normally. Cones appeared normal during the time of retinal development and maturation and it was not until the age of 2-3 years (Narfström and Nilsson, 1986, Incest. Ophthalmol, Vis. Sci. 27, 1569-76) that degenerative changes were seen also in cones.

Aging↗
PubMedDate not supplied

A molecular view of vertebrate retinal development.

Immunological probes have begun to identify molecules that delineate cell layers and cell types during the formation of the retina and other parts of the optic cup. Within the developing retina, cell-type-specific monoclonal antibodies have been used to show that differentiation occurs before cells reach their final laminar position. Cell surface molecules have been found expressed in position-dependent gradients across the retina. These molecules may convey positional information to the retinal cells and their topographic connections. One such molecule is a modified carbohydrate group on a ganglioside, suggesting that such groups may play a role in neural development. A variety of molecules that are expressed by rod photoreceptors at defined stages of their differentiation have been characterized. These molecules have been used to show the development of subcellular compartments within rods. In vitro studies have suggested that photoreceptor molecules expressed at different times are under different forms of regulation. Some of these cell-specific molecules have been shown to be under transcriptional control and thus defined cell interactions seem to be linked to changes in gene expression during retinal development.

Aging↗
PubMed2001

Asymmetric segregation of Numb in retinal development and the influence of the pigmented epithelium.

Asymmetric segregation of cell-fate determinants during cytokinesis plays an important part in controlling cell-fate choice in invertebrates. During Drosophila neurogenesis, for example, asymmetric segregation of the Numb protein, which inhibits Notch signaling, is necessary for the two daughter cells of a division to have different fates. In vertebrates, the role of asymmetric segregation of cell-fate determinants is uncertain, and the way the process might be regulated is unknown. We have studied the orientation of cell divisions and the distribution of Numb in the developing rat retina. We show that, whereas most retinal neuroepithelial cells divide with their mitotic spindles oriented parallel to the plane of the neuroepithelium, a substantial minority divides with their spindles oriented perpendicularly. The proportion of these vertically dividing cells changes during development, peaking around the day of birth. Numb appears to be inherited only by the apical daughter cell when a neuroepithelial cell divides vertically. Similarly, in dissociated cell cultures, some retinal neuroepithelial cells divide asymmetrically and distribute Numb to only one of the two daughter cells, suggesting that the dissociated cells can retain their polarity in vitro. Using retinal explant cultures, we find that the retinal pigment epithelium apparently promotes vertical divisions in the neural retina. To our knowledge, this is the first evidence that asymmetric segregation of cell-fate determinants may contribute to cell diversification in the mammalian retina and that an epithelium controls this process by influencing the plane of division in the adjacent neural retina.

Animals↗
PubMed1996

Influence of spontaneous activity and visual experience on developing retinal receptive fields.

BACKGROUND: The role played by early neural activity in shaping retinal functions has not yet been established. In the developing vertebrate retina, ganglion cells fire spontaneous bursts of action potentials before the onset of visual experience. This spontaneous bursting disappears shortly after birth or eye opening. In the present study, we have investigated whether the outgrowth of receptive fields in turtle retinal ganglion cells is affected by early spontaneous bursting or by early visual experience. RESULTS: Ganglion cells normally stop bursting spontaneously 2-4 weeks post-hatching, the time when receptive-field areas reach adult size. When turtles are reared in the dark, the spontaneous bursting persists. Concomitantly, receptive-field areas expand to more than twice those observed in normal adults. To test whether chronic blockade of spontaneous bursting inhibits the expansion of developing receptive-field areas, we have exposed the retina to curare, a nicotinic cholinergic antagonist, because spontaneous bursting by ganglion cells requires acetylcholine. Curare was released from Elvax, a slow-release polymer that was implanted in the eye. When spontaneous bursting was chronically blocked with curare in hatchlings, dark-induced expansion of receptive fields was abolished. Moreover, receptive fields of ganglion cells exposed to curare in hatchlings reared in normal light and dark cycles were smaller than normal. CONCLUSIONS: These results strongly suggest that early, acetylcholine-dependent spontaneous bursts of activity control the outgrowth of receptive-field areas in retinal ganglion cells. The onset of visual experience induces the disappearance of the immature spontaneous bursts, resulting in the stabilization of receptive-field areas to their mature size.

Animals↗
PubMed2005

The renin-angiotensin system and the developing retinal vasculature.

PURPOSE: To determine the location and activity of renin-angiotensin system (RAS) components in the developing rat retina and whether the RAS influences retinal vascularization. METHODS: Transgenic Ren-2 rats, which overexpress the RAS, and Sprague-Dawley (SD) rats were studied at postnatal day (P)1, P7, P14, P21, and P90. Immunohistochemistry was performed for angiotensinogen, prorenin, angiotensin II (Ang II), and the angiotensin type 1 (AT(1)) and 2 (AT(2)) receptors. Retinal active renin and prorenin were measured by radioimmunoassay, and the density of angiotensin-converting enzyme (ACE) by autoradiography. At P1 to P7, Ren-2 and SD rats were administered either the ACE inhibitor lisinopril (10 mg/kg per day, intraperitoneally [IP]) or the AT(1) receptor antagonist losartan (10 mg/kg per day, IP), and vessel length and density were measured. RESULTS: At all time points, RAS components were localized to blood vessels and cells in the ganglion cell layer. At P1, Ang II and both the AT(1) and AT(2) receptors were on hyaloid vessels. ACE binding increased in intensity from P1 to P90. Retinal renin was mainly activated and was 5- to 15-fold higher in Ren-2 than in SD rats. In Ren-2 rats, the growing vasculature extended farther into the retinal periphery than in SD rats and was unchanged with either lisinopril or losartan. Vascular density was increased in the periphery of Ren-2 rats compared with SD rats and was reduced with lisinopril but not with losartan. CONCLUSIONS: In the developing rat retina, a complete RAS is mainly found in blood vessels and cells in the ganglion cell layer, where it may influence the early stages of vascularization.

Angiotensin II↗
PubMed1994

RETINOIC ACID MODULATES RETINAL DEVELOPMENT IN THE JUVENILES OF A TELEOST FISH

Small (<30 g) juvenile rainbow trout (Oncorhynchus mykiss) possess retinal photoreceptor mechanisms sensitive to light in the near ultraviolet, short (blue), middle (green) and long (red) wavelengths. During normal development, the ultraviolet cone mechanism gradually disappears until, by approximately 60&shy;80 g, individuals are no longer sensitive in the ultraviolet. This shift in spectral sensitivity is associated with the loss of a single class of photoreceptor cells &shy; small accessory corner cones &shy; from the retinal photoreceptor cell mosaic. Treating small (<15 g) rainbow trout with 10(-6) mol l-1 all-trans retinoic acid (20 min exposure by immersion) induced a precocial loss of ultraviolet photosensitivity and an associated change in the retinal photoreceptor cell mosaic only 2 weeks after treatment. These changes were indistinguishable from the events that occur during normal development. Six weeks after exposure to retinoic acid, large (>90 g) rainbow trout, which had lost their ultraviolet cones during normal development, were once again ultraviolet-photosensitive and small accessory corner cones were found in their retinas. These results imply that the ultraviolet-sensitive cones, although lost at one point during development, can reappear at another time during the life history of the same individual. Retinoic acid is involved in these morphogenetic processes.

Journal Article↗
PubMed1997

Evidence for multiple, local functions of ciliary neurotrophic factor (CNTF) in retinal development: expression of CNTF and its receptors and in vitro effects on target cells.

There is increasing, although largely indirect, evidence that neurotrophic factors not only function as target-derived survival factors for projection neurons, but also act locally to regulate developmental processes. We studied the expression of ciliary neurotrophic factor (CNTF) and the CNTF-specific ligand-binding alpha-subunit of the CNTF receptor complex (CNTFR alpha) in the rat retina, a well-defined CNS model system, and CNTF effects on cultured retinal neurons. Both CNTF and CNTFR alpha (mRNA and protein) are expressed during phases of retinal neurogenesis and differentiation. Retina-specific Müller glia are immunocytochemically identified as the site of CNTF production and CNTFR alpha-expressing, distinct neuronal cell types as potential CNTF targets. Biological effects on corresponding neurons in culture further support the conclusion that locally supplied CNTF plays a regulatory role in the development of various retinal cell types including ganglion cells and interneurons.

Animals↗
PubMed2002

mRNA expression of the murine glycoprotein (transmembrane) nmb (Gpnmb) gene is linked to the developing retinal pigment epithelium and iris.

The murine homologue of the human glycoprotein (transmembrane) NMB (GPNMB) gene was identified by subtractive cloning from in vitro cultured murine primary osteoblast cells and subsequent RACE-PCR. GPNMB is a highly glycosylated type I transmembrane protein that shares significant sequence homology to several melanosomal proteins. Increasing expression of Gpnmb mRNA was observed during differentiation of murine primary osteoblast cell cultures. To address the potential functions of GPNMB we analysed its mRNA-expression during murine embryonic development. In early development Gpnmb mRNA is detected at high levels in the outer layer of the retina. Later in development expression gets restricted to the retinal pigment epithelium and iris. At the cytoplasmic domain of GPNMB, a conserved di-leucin-based endosomal/melanosomal-sorting signal (ExxPLL) was located, present as well in several known melanosomal proteins. To analyse the subcellular localization we used EGFP-tagged GPNMB transfected in COS7 and HEK293 cells. In both non-pigmented cell lines, the EGFP-GPNMB fusion protein was localized to vesicular, endosomal like structures. Sequence homology to known melanosomal proteins, mRNA expression and subcellular localization are suggestive for GPNMB as an intracellular, endosomal/melanosomal compartment specific protein important for melanin biosynthesis and the development of the retinal pigment epithelium and iris. As the gene coding for human GPNMB was localized to chromosome 7p15, a locus involved in the human inherited disease cystoid macular edema, also known as dominant cystoid macular dystrophy (OMIM 153880) we highly suggest that GPNMB is a candidate gene for this human inherited disease.

Animals↗
PubMed2003

Expression of the cyclin-dependent kinase inhibitor p27Kip1 by developing retinal pigment epithelium.

The cyclin-dependent kinase (Cdk) inhibitor p27Kip1 contributes to the timing of cell cycle withdrawal during development and, consequently, in organogenesis. Within the retina, this effector protein is up-regulated during the birth of neuronal and glial cells [Dev. Biol. (2000) 299]. However, its expression within the retinal pigment epithelium (RPE), a supporting cell layer that is essential for neural retina development and function, has not previously been reported. We show that p27Kip1 protein expression in the RPE occurs in two phases: an up-regulation during mid-to late embryonic stages and a down-regulation during the subsequent postnatal period. In the early phase of up-regulation, an inverse relationship is seen between expression of p27Kip1 and PCNA, an indicator of cycling cells. During both up-and down-regulation, the change in spatial pattern of expression proceeds in a central to peripheral manner, with p27Kip1 up-regulation paralleling retinal maturation. These data suggest that this cell cycle regulator may be an important factor controlling the timing of RPE cell cycle withdrawal.

Animals↗
PubMed1991

Differential effects of laminin and merosin on neurite outgrowth by developing retinal ganglion cells.

In previous work, we showed that cultured avian embryonic retinal ganglion cells (RGC) extend neurites on EHS-laminin early in development, but lose this ability with maturation, as a result of a sharp decline in laminin receptor numbers. Here we show that EHS-laminin promotes neurite outgrowth also from embryonic mammalian RGC, in contrast to previous reports, and that these exhibit similar age-dependent growth responses on laminin. Antibody blocking studies show that this behaviour is mediated in mouse RGC by alpha 6 beta 1 integrin dimers. The laminin isoform merosin is also effective as a neurite outgrowth-promoting substrate for RGC but differs in its ability to elicit a response at advanced stages of development (up to hatching in the chick). Neurite outgrowth by RGC on merosin is inhibited, at all ages, by the function-blocking, anti-beta 1 integrin antibody, CSAT, suggesting that these neurons use alternative alpha beta 1 dimers in their interactions with EHS-laminin and merosin. Together, these findings emphasise the generality of the responsiveness of vertebrate embryonic RGC to laminin during development, and reveal interesting differences in the effects of laminin variants on CNS axon growth and regeneration.

Animals↗
PubMed2001

Signalling pathways in Drosophila and vertebrate retinal development.

The near-catholic conservation of paired box gene 6 (Pax6) and its supporting cast of retinal determination genes throughout the animal kingdom has sparked a scientific war over the evolutionary origins of the eye. The battle pits those who support a polyphyletic history for the eye against those who argue for a common ancestor for all 'seeing' animals. Recent papers have shed light on how eyes in both vertebrates and invertebrates are patterned. New insights into the roles that signal-transduction cascades might have in determining the Drosophila melanogaster eye indicate that, like many developmental processes, eye specification is an inductive process.

Animals↗
PubMed1996

Measuring visual function and quality of life in patients with cytomegalovirus retinitis. Development of a questionnaire. Studies of Ocular Complication of AIDS Research Group.

OBJECTIVE: To develop and test a brief questionnaire designed to assess visual symptoms, visual function in daily activities, and impact of treatment administration in patients with cytomegalovirus retinitis related to acquired immunodeficiency syndrome. DESIGN: Observational cross-sectional study. Patients were recruited in June and July 1992. SETTING: Seven university-based sites participating in the Studies of Ocular Complications of AIDS. PATIENTS: Twenty-six subjects enrolled in a randomized trial that compared foscarnet and ganciclovir for the treatment of cytomegalovirus retinitis. MAIN OUTCOME MEASURES AND ANALYSIS: Distributions of scores, reliability, and validity of newly developed scales to assess visual function, visual symptoms, and global vision. Spearman rank correlations with 95% confidence intervals were used to test hypothesized relationships between scale scores, visual acuity, visual field, and findings from visual examination. RESULTS: The final 18-item self-administered questionnaire required 5 minutes to complete. The new scales had high internal consistency (Cronbach alpha = .81 to .94). As hypothesized, patient-reported vision scores decreased with greater abnormalities found on ophthalmologic examination. Visual symptoms were most strongly related to findings in the worse eye. Visual function and global vision scores were moderately correlated with findings from visual testing and examination, and less strongly related to general health perceptions. Patients reported considerable impairment: 42% reported blurred vision; 40%, difficulty reading; 44%, difficulty driving; and 40%, that treatment interfered with social activities; 50% reported substantial trouble with their vision. CONCLUSIONS: The brief questionnaire developed to assess patient-reported visual function in cytomegalovirus retinitis appears reliable and valid as a measure of performance of vision-related activities, visual symptoms, and the impact of treatment administration. Further research is needed to test its utility as an outcome measure in longitudinal studies of cytomegalovirus retinitis.

AIDS-Related Opportunistic Infections↗