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PubMed1978

Vitreous findings in fellow eyes of aphakic retinal detachment.

One hundred patients had bilateral aphakia, primary rhegmatogenous retinal detachment, and adequate visualization of the retinal and vitreous in the fellow eye. Of 43 patients with posterior vitreous separation and no retinal tear in the fellow eye, only one (2%) subsequently developed retinal detachment. Of 40 patients without posterior vitreous separation in the fellow eye, eight (20%) later developed retinal detachment following posterior vitreous separation. The remaining 17 patients had posterior vitreous separation and retinal tear or detachment at the time of initial examination. Thus, if posterior vitreous separation occurs without forming retinal tear, the risk of developing retinal detachment is significantly lowered.

Adult↗
PubMed1997

Immunolocalization of transforming growth factor-alpha and its receptor in the normal and hyperoxia-exposed neonatal rat retina.

PURPOSE: Transforming growth factor-alpha (TGF-alpha) is a mitogenic polypeptide for a variety of different cells types including retinal neurons and glial cells. We have examined the temporal and spatial expression of TGF-alpha and its receptor in the normal and hyperoxia-exposed neonatal rat retina to determine if the expression is consistent with a role in retinal development and response to retinal injury. METHODS: We have used immunohistochemistry to examine TGF-alpha and epidermal growth factor receptor (EGF-R) on postnatal days (1, 5, 10, 14, 18, and 25). To examine TGF-alpha and EGF-R expression after retinal injury we studied the retinas from rats which were exposed to 80% oxygen for 10 days and then recovered in room air. Immunolocalization of type IV collagen was performed to examine the retinal vasculature development after hyperoxia. RESULTS: The pattern of TGF-alpha and EGF-R expression in the neural retina evolved from a diffuse pattern on postnatal day 1 to restricted sites on postnatal day 14. The TGF-alpha immunoreactivity was consistent with localization in Müller cells on postnatal day 14. Both TGF-alpha and EGF-R patterns were altered in the retinas from rats that had been exposed to hyperoxia and recovered in room air for 4 days. The type IV confirmed immunostaining confirmed vaso-obliteration in the deep layer of retinal vessels after hyperoxia. CONCLUSIONS: Our findings of altered expression of TGF-alpha and EGF-R during retinal development suggests a biological function for this growth factor, possibly promoting retinal cell proliferation, differentiation, and survival. The altered immunolocalization of TGF-alpha and EGF-R in the hyperoxia-exposed retina suggest that TGF-alpha is likely involved in the retinal response to injury.

Animals↗
PubMed2001

Symptoms predictive for the later development of retinal breaks.

OBJECTIVE: To identify symptoms in patients with isolated posterior vitreous detachment predictive for the later development of retinal breaks. METHODS: Two hundred eighty consecutive patients seen with symptoms of posterior vitreous detachment were prospectively asked to complete a questionnaire detailing their symptoms. At the time of presentation and follow-up, all patients had a full ophthalmologic examination including slitlamp biomicroscopy with Goldmann 3-mirror contact lens after maximal pupil dilatation. Two hundred fifty patients with an isolated posterior vitreous detachment were included and reexamined 6 weeks after the onset of symptoms. If small retinal or vitreous hemorrhages were detected, patients were reexamined after 2 weeks. RESULTS: In 13 patients (5.2%) a retinal break was detected at reexamination. Logistic regression analysis with backward elimination revealed that symptoms of flashes in combination with clouds or multiple (>10) small dots at the time of the initial examination or an increase of floaters after the initial examination were statistically significantly (P<.001) related to the development of new breaks. These symptoms had a predictive value for the presence or absence of a new retinal break of 75.0% and 99.6%, respectively. CONCLUSIONS: Specific symptoms can identify patients at risk for the development of new retinal breaks after an initial examination in which no abnormalities were found and may obviate the need for follow-up appointments of patients not at risk.

Diagnostic Techniques, Ophthalmological↗
PubMed1981

Effect of monosodium glutamate on retinal vessel development and permeability in rats.

Monosodium glutamate (MSG) administered to neonatal rats on postnatal days 1 to 10 caused a generalized degeneration of the inner retinal layers. MSG administered only on postnatal days 8, 9, 10, and/or 11 caused a retinopathy limited to more peripheral retinal areas corresponding to currently existing regions of immature retinal vessels. Ink-injected retinal vessel studies showed a delay in development of the retinal vessel network but no alterations in vessel patency. Fluorescence microscopic examination of freeze-dried tissues revealed to abnormalities of the blood-retinal barriers to sodium fluorescein. We conclude, as demonstrated by these methods, that MSG retards development of the retinal vessels but does not affect development of the blood-retinal barriers. The retinotoxic effect of MSG apparently results from a mechanism(s) other than a breakdown of the blood-retinal barrier.

Age Factors↗
PubMed1999

The posterior vitreous detachment clinic: do new retinal breaks develop in the six weeks following an isolated symptomatic posterior vitreous detachment?

PURPOSE: Symptomatic posterior vitreous detachment (PVD) is sometimes associated with sight-threatening retinal tears or retinal detachment. Patients are usually reviewed twice because it is believed that retinal breaks may develop within 6 weeks of a PVD and as such the management of a PVD consumes significant resources. The aim of this study was to find the frequency of retinal breaks developing within 6 weeks of an isolated PVD using the same experienced examiner at both visits. METHOD: Patients presenting to the eye casualty with symptomatic PVD were examined by the casualty staff. Those with a retinal break or retinal detachment were referred directly for treatment and those with only a PVD were seen within 8 days in the PVD clinic. They were examined by a vitreo-retinal Fellow using indirect ophthalmoscopy and a 20 D lens with scleral indentation. The position and nature of any retinal abnormalities were noted and compared with those described in the casualty notes. Those with sight-threatening breaks were referred for treatment and the remainder were reviewed 5 weeks later when the presence of any new breaks was noted. RESULTS: One hundred and seven patients were referred to the PVD clinic over a 6-month period, of whom 2 did not have a PVD. At the first visit to the PVD clinic 6 patients had round holes anterior to the equator, 2 had equatorial horseshoe tears and 1 had lattice with holes. At the second visit, 2 additional patients had round holes anterior to the equator but in both the retina had been obscured by vitreous haemorrhage at the first visit. No patient in whom a full examination was possible at the first visit developed further retinal pathology. CONCLUSION: These results demonstrate the need to perform a full examination of the peripheral retina with scleral indentation at the time of presentation and emphasise the importance of finding a vitreous haemorrhage following a symptomatic PVD. If no retinal breaks are detected by thorough examination at presentation, further reviews, in the absence of increasing symptoms, may not be necessary.

Adult↗
PubMed2006

The CNTF/LIF signaling pathway regulates developmental programmed cell death and differentiation of rod precursor cells in the mouse retina in vivo.

Natural cell death is critical for normal development of the nervous system, but the extracellular regulators of developmental cell death remain poorly characterized. Here, we studied the role of the CNTF/LIF signaling pathway during mouse retinal development in vivo. We show that exposure to CNTF during neonatal retinal development in vivo retards rhodopsin expression and results in an important and specific deficit in photoreceptor cells. Detailed analysis revealed that exposure to CNTF during retinal development causes a sharp increase in cell death of postmitotic rod precursor cells. Importantly, we show that blocking the CNTF/LIF signaling pathway during mouse retinal development in vivo results in a significant reduction of naturally occurring cell death. Using retroviral lineage analysis, we demonstrate that exposure to CNTF causes a specific reduction of clones containing only rods without affecting other clone types, whereas blocking the CNTF/LIF receptor complex causes a specific increase of clones containing only rods. In addition, we show that stimulation of the CNTF/LIF pathway positively regulates the expression of the neuronal and endothelial nitric oxide synthase (NOS) genes, and blocking nitric oxide production by pre-treatment with a NOS inhibitor abolishes CNTF-induced cell death. Taken together, these results indicate that the CNTF/LIF signaling pathway acts via regulation of nitric oxide production to modulate developmental programmed cell death of postmitotic rod precursor cells.

Animals↗
PubMed1986

Cell death in the development of the human retina: phagocytosis of pyknotic and apoptotic bodies by retinal cells.

Apoptosis is a natural form of cell death and has features in common with aspects of cell deletion observed in the course of human retinal development. In this report, we describe the occurrence of apoptotic cells in various layers of the developing retina. Pyknotic residues were observed within phagosomes of neighbouring retinal cells. Our observations imply that most of the debris resulting from cell death is taken up by adjacent tissue cells rather than by mononuclear phagocyte series cells (macrophages) during early stages of human retinal development.

Cell Nucleus↗
PubMed2003

Retinal vascular development and oxygen-induced retinopathy: a role for adenosine.

Adenosine is a ubiquitous molecule that is produced predominantly by catabolism of adenosine triphosphate. Levels of this nucleoside increase dramatically with ischemia and elevated tissue activity. Adenosine levels are high in inner retina during retinal vascular development in postnatal dog. The source appears to be the ectoenzyme 5' nucleotidase, which is prominent at this time in the innermost process of Muller cells. One of the adenosine receptors, A(2A), is present on endothelial cell precursors, angioblasts, and endothelial cells in formed blood vessels in neonatal dog. These observations suggest that adenosine is important in retinal vascular development. Oxygen-induced retinopathy (OIR) is a model for human retinopathy of prematurity (ROP). The initial event in OIR is induced by exposure of the developing retina to high oxygen. Vascular development is halted and over 60% of the retinal vasculature is lost during this stage of the disease in dog, which is called vaso-obliteration. 5' nucleotidase is dramatically reduced during vaso-obliteration, resulting in a sharp decline in adenosine. When animals are returned to room air, the retina is hypoxic because of the lack of blood vessels, oxygen consumption is increased due to neuronal development, and systemic levels of oxygen have returned to normal. At this time, 5' nucleotidase activity and adenosine levels are elevated well beyond normal levels. This stage of OIR is the vasoproliferative stage and A(2A) expression and endothelial cell proliferation are very elevated compared to control animals. Florid preretinal neovascularization forms, which has high levels of adenosine and A(2A) receptors. Therefore, adenosine and its A(2A) receptor appear to be important in canine OIR. This work suggests that adenosine and its receptors may be a therapeutic target in OIR. This hypothesis is supported by recent studies in mouse (Mino et al., Invest. Ophthalmol. Vis. Sci. 42(13) (2001) 3320), which demonstrated that targeting one of the A(2) receptors can inhibit formation of neovascularization in OIR.

Adenosine↗
PubMed2006

The Rx-like homeobox gene (Rx-L) is necessary for normal photoreceptor development.

PURPOSE: The retinal homeobox (Rx) gene plays an essential role in retinal development. An Rx-like (Rx-L) gene from Xenopus laevis has been identified. The purpose of this study was to analyze the function of Rx-L in the developing retina. METHODS: DNA-binding properties of Rx-L were analyzed by electrophoretic mobility shift assay (EMSA), with in vitro-translated proteins and radiolabeled oligonucleotide probe. The Rx-L expression pattern was analyzed by in situ hybridization using whole or sectioned embryos and digoxigenin-labeled antisense riboprobes. Rx-L loss of function was studied by using antisense morpholino oligonucleotides targeted to the Rx-L translation initiation site. Embryos injected with control or Rx-L morpholinos were analyzed at stage 41 or 45. RESULTS: Rx-L shares homology with Rx at the homeo-, OAR, and Rx domains, but lacks an octapeptide motif. Rx-L is expressed in the developing retina beginning in the early tailbud stage. In the maturing retina, Rx-L expression is restricted primarily to the developing photoreceptor layer and the ciliary marginal zone. Rx-L can bind a photoreceptor conserved element-1 (PCE-1) oligonucleotide, an element conserved among all known photoreceptor gene promoters. In a promoter activity assay, Rx-L functions as a stronger transcriptional activator than Rx. Antisense morpholino-mediated knockdown of Rx-L expression resulted in a decrease in rhodopsin and red cone opsin expression levels in Xenopus retinas. Injection of the Rx-L antisense morpholino oligonucleotide also resulted in a decrease in the length of both rod and cone outer segments. CONCLUSIONS: The results suggest that Rx-L functions to regulate rod and cone development by activating photoreceptor-specific gene expression.

Amino Acid Sequence↗
PubMed1999

Retinal complications after cataract extraction in patients with high myopia.

OBJECTIVE: To assess risk factors and incidence of retinal complications after cataract extraction in patients with high myopia. DESIGN: Retrospective, noncomparative case series. PARTICIPANTS: One hundred eighteen patients with highly myopic eyes who had an axial length of 26 mm or more (mean axial length, 30.13 +/- 2.08 mm) and who underwent cataract surgery over a period of 6 years were studied. INTERVENTION: Patients underwent cataract extraction either by extracapsular cataract extraction (ECCE) or phacoemulsification. Prophylactic argon laser photocoagulation was performed in 13 eyes for retinal tears recognized before surgery and in 13 eyes after surgery; neodymium:YAG (Nd:YAG) laser capsulotomy was performed for patients with posterior capsule opacification (PCO) that affected the vision. MAIN OUTCOME MEASURES: Incidence of retinal detachment and PCO and percentage of prophylactic argon laser or of Nd:YAG laser treatments. RESULTS: Of the 118 eyes, 73 (61.9%) underwent ECCE and 45 (38.1%) underwent phacoemulsification. Posterior capsule opacification was the most common complication and was found in 30 eyes (25.4%). Thirteen patients (11%) received prophylactic laser treatment for retinal tears before cataract operation, and 13 more patients (11%) had postoperative retinal tears requiring laser treatments. None of these patients developed retinal detachment. Two patients (1.69%) developed retinal detachment within 6 months after their operations. There were no intraoperative complications, and postoperative Nd:YAG capsulotomy was not performed in these two patients. CONCLUSIONS: Active searching and prophylactic laser treatments for retinal tears developed before and after cataract extraction in patients with high myopia are recommended. This may lower the incidence of postoperative retinal detachment.

Adult↗
PubMed2006

TrkB/BDNF signaling regulates photoreceptor progenitor cell fate decisions.

Neurotrophins, via activation of Trk receptor tyrosine kinases, serve as mitogens, survival factors and regulators of arborization during retinal development. Brain-derived neurotrophic factor (BDNF) and TrkB regulate neuronal arborization and survival in late retinal development. However, TrkB is expressed during early retinal development where its functions are unclear. To assess TrkB/BDNF actions in the early chick retina, replication-incompetent retroviruses were utilized to over-express a dominant negative truncated form of TrkB (trunc TrkB), or BDNF and effects were assessed at E15. Clones expressing trunc TrkB were smaller than controls, and proliferation and apoptosis assays suggest that decreased clone size correlated with increased cell death when BDNF/TrkB signaling was impaired. Analysis of clonal composition revealed that trunc TrkB over-expression decreased photoreceptor numbers (41%) and increased cell numbers in the middle third of the inner nuclear layer (INL) (23%). Conversely, BDNF over-expression increased photoreceptor numbers (25%) and decreased INL numbers (17%). Photoreceptors over-expressing trunc TrkB demonstrated no increase in apoptosis nor abnormalities in lamination suggesting that TrkB activation is not required for photoreceptor cell survival or migration. These studies suggest that TrkB signaling regulates commitment to and/or differentiation of photoreceptor cells from retinal progenitor cells, identifying a novel role for TrkB/BDNF in regulating cell fate decisions.

Animals↗
PubMed2006

Attenuation of retinal vascular development and neovascularization in transgenic mice over-expressing thrombospondin-1 in the lens.

Thrombospondin-1 (TSP1) is an endogenous inhibitor of angiogenesis and induces endothelial cell (EC) apoptosis. To study the role TSP1 plays during vascular development and neovascularization, we assessed the effects of ectopic TSP1 expression in the lens on retinal vascularization in transgenic mice. The TSP1 over-expressing mice showed abnormalities in the development of retinal vasculature. There was a dramatic decrease in the density of superficial and deep vascular plexuses of the retina in transgenic mice. The retinal vessels in TSP1 transgenic mice also appeared nonuniform and abnormal in maturation. We detected an increase in the number of EC undergoing apoptosis, which was compensated, in part, by an increase in cell proliferation in retinal vasculature of TSP1 transgenic mice. The TSP1 transgenic mice also exhibited increased levels of vessel obliteration and a limited preretinal neovascularization during oxygen-induced ischemic retinopathy (OIR). Our results indicate increased expression of TSP1 attenuates normal retinal vascularization and preretinal neovascularization during OIR. Therefore, modulation of TSP1 expression may provide an effective mechanism for regulation of ocular angiogenesis.

Animals↗
PubMed1996

[Severe myopia and delivery].

AIM: There has been concern that patients with high myopia are at a risk of developing retinal tears as they go through a spontaneous delivery. Therefore the aim of the paper was to examine retinal changes in the group of female patients with high myopia before and after delivery. MATERIAL AND METHODS: Eye examinations were performed before and after delivery in two groups of patients: 42 patients with high myopia and 4 patients with high myopia and retinal detachment surgery in one eye. RESULTS: There was no progression of retinal changes and development of retinal tears, but in some patients retinal hemorrhages and macular edema were observed. CONCLUSIONS: High myopia is not the indication for the cesarean section, but the patients should be examined after the delivery.

Adult↗
PubMed2001

Development of retinal ganglion cell structure and function.

In this review, we summarize the main stages of structural and functional development of retinal ganglion cells (RGCs). We first consider the various mechanisms that are involved in restructuring of dendritic trees. To date, many mechanisms have been implicated including target-dependent factors, interactions from neighboring RGCs, and afferent signaling. We also review recent evidence showing how rapidly such dendritic remodeling might occur, along with the intracellular signaling pathways underlying these rearrangements. Concurrent with such structural changes, the functional responses of RGCs also alter during maturation, from sub-threshold firing to reliable spiking patterns. Here we consider the development of intrinsic membrane properties and how they might contribute to the spontaneous firing patterns observed before the onset of vision. We then review the mechanisms by which this spontaneous activity becomes correlated across neighboring RGCs to form waves of activity. Finally, the relative importance of spontaneous versus light-evoked activity is discussed in relation to the emergence of mature receptive field properties.

Animals↗
PubMed2004

Cell type-specific effects of Rb deletion in the murine retina.

Certain cells of the human retina are extremely sensitive to loss of function of the retinoblastoma tumor suppressor gene RB. Retinoblastomas develop early in life and at high frequency in individuals heterozygous for a germ-line RB mutation, and sporadic retinoblastomas invariably have somatic mutation in the RB gene. In contrast, retinoblastomas do not develop in Rb+/- mice. Although retinoblastoma is thought to have developmental origins, the function of Rb in retinal development has not been fully characterized. Here we studied the role of Rb in normal retinal development and in retinoblastoma using conditional Rb mutations in the mouse. In late embryogenesis, Rb-deficient retinas exhibited ectopic S-phase and high levels of p53-independent apoptosis, particularly in the differentiating retinal ganglion cell layer. During postnatal retinal development, loss of Rb led to more widespread retinal apoptosis, and adults showed loss of photoreceptors and bipolar cells. Conditional Rb mutation in the retina did not result in retinoblastoma formation even in a p53-mutant background. However, on a p107- or p130-deficient background, Rb mutation in the retina caused retinal dysplasia or retinoblastoma.

Animals↗
PubMed1987

Role of cell death in the topogenesis of neuronal distributions in the developing cat retinal ganglion cell layer.

The neurons of the developing and adult ganglion cell layer of the cat retina may be morphologically divided into two major populations. One population, the classic neurons, is mainly composed of ganglion cells, and of a small percentage of displaced amacrines, the bar cells. The remaining neurons are microneurons, which make up the majority of the displaced amacrine population. The loss of ganglion cells during the development has been attributed to cell death. It has alternatively been suggested that some ganglion cells may lose their axon and be transformed into displaced amacrine cells, without degeneration of the cell soma. Reexamination of foetal and postnatal cat retinas confirms the presence of degenerating cells in the ganglion cell layer. Their number appears to be at a maximum on embryonic day (E) 57 but declines rapidly until birth. The peak of cell death thus coincides with the decline in optic nerve fibre counts and classical neuron or ganglion cell numbers. Some cells in early stages of degeneration resemble classical neurons, but the original morphology of those advanced stages of degeneration could not be identified, nor was it possible to identify pyknotic microneurons at any stage. Substantial degeneration of the microneurons is not suggested but if it occurs, it is masked by an overall increase in the population of these cells before birth. Cell death in the microneuron population thus cannot yet be ruled out. It has been argued in the literature that fragments of degenerating cells in developing neural tissue are cleared by microglia within 10-14 hours. In order to test the hypothesis that operation of cell death can alone account for the observed loss of classical neurons in the foetal cat retina, we have modelled the effect of various presumed clearance times on corresponding neuronal population magnitudes. It is found that a constant clearance time of 10-24 hours would be consistent with the observed loss of classical neurons before birth. If this is true, then no ganglion cells would remain for transformation into amacrine cells. The absolute density of degenerating or pyknotic cells is found to be relatively constant across the retina. However their density expressed as a percentage of the local population of classical neurons is markedly higher in peripheral than central retina. In the former region, they compose more than 10% of classical neurons at stage E57. On the same day, the percentage distribution maps define an elongated central area containing only 3-5% pyknotic profiles. This region corresponds to the location of the future visual streak.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

The effect of raised inspired carbon dioxide on developing rat retinal vasculature exposed to elevated oxygen.

Hyperoxia is a risk factor for retinopathy of prematurity (ROP), a blinding disease in infants. However, ROP develops in human infants without raised arterial oxygen levels, such as in cyanotic congenital heart disease. In these infants raised pCO2 may be a risk factor. We investigated the effect of inspired CO2 on oxygen induced retinopathy in the rat. 56 newborn Sprague-Dawley rats were exposed to high cyclical O2 for seven days. In a control group, 27 rats were exposed to negligible CO2 by the use of soda lime. In the high CO2 group, 29 rats were exposed to elevated CO2 by omitting soda lime from their chambers. Rats in both groups had a recovery period of three days in room air following cyclical O2 exposure. On the eleventh day all rats were sacrificed after intracardiac injections of fluorescein under deep anesthesia and the retinae were dissected and flat mounted for fluorescent microscopy. The ratio of vascularized:total retinal area was calculated using computer assisted image analysis. In the high CO2 group 62% +/- 7% SD of the retina was vascularized vs. 81% +/- 7% in low CO2 group (p < 0.001). Elevated inspired CO2 results in pronounced retardation of retinal vascular development in neonatal rats exposed to fluctuating raised oxygen.

Animals↗