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PubMed1989

Analysis of proteins in developing rd (retinal degeneration) chick retina using two-dimensional gel electrophoresis.

The rd (retinal degeneration) chick possesses an autosomal recessive mutation which results in behavioral and electrophysiological blindness at hatch. Using the technique of two-dimensional gel electrophoresis, we have identified two groups of proteins whose expression in the retina/pigment epithelium/choroid (RET/PE/CH) of +/+, +/rd and rd/rd chicks is related to genotype. The two proteins within Group 1 had an apparent mass (Mr) of 63 kDa and isoelectric points (pI) of 6.48 and 6.55. The four proteins in Group 2 had an apparent Mr of 98 kDa and pI values ranging from 6.08 to 6.25. Quantities of the Group 1 proteins in RET/PE/CH of each of the three types of animals were found to be related to genotype; the amounts of each did not change with development. The expression of the Group 2 proteins in PET/PE/CH was found to change during retinal development. Proteins P98-6.08 (Mr-pI) and P98-6.13 were found in all rd/rd and +/rd RET/PE/CH and in most +/+ embryonic tissues. Proteins P98-6.19 and P98-6.25, which were present in the majority of +/+ embryonic and in all +/+ E21 (hatch RET/PE/CH, did not appear in +/rd tissues until hatch. P98-6.19 and P98-6.25 were never observed in rd/rd RET/PE/CH.

Animals↗
PubMed1998

Basic fibroblast growth factor is neither necessary nor sufficient for the development of retinal neovascularization.

Basic fibroblast growth factor (FGF2) is constitutively expressed in the retina and its expression is increased by a number of insults, but its role in the retina is still uncertain. This study was designed to test the hypothesis that altered expression of FGF2 in the retina affects the development of retinal neovascularization. Mice with targeted disruption of the Fgf2 gene had no detectable expression of FGF2 in the retina by Western blot, but retinal vessels were not different in appearance or total area from wild-type mice. When FGF2-deficient mice were compared with wild-type mice in a murine model of oxygen-induced ischemic retinopathy, they developed the same amount of retinal neovascularization. Transgenic mice with a rhodopsin promoter/Fgf2 gene fusion expressed high levels of FGF2 in retinal photoreceptors but developed no retinal neovascularization or other abnormalities of retinal vessels; in the ischemic retinopathy model, they showed no significant difference in the amount of retinal neovascularization compared with wild-type mice. These data indicate that FGF2 expression is not necessary nor sufficient for the development of retinal neovascularization. This suggests that agents that specifically antagonize FGF2 are not likely to be useful adjuncts in the treatment of retinal neovascularization and therapies designed to increase FGF2 expression are not likely to be complicated by retinal neovascularization.

Animals↗
PubMedDate not supplied

Expression of transforming growth factor-beta superfamily receptors in developing rat eyes.

PURPOSE: To ascertain the role played by the transforming growth factor (TGF)-beta superfamily in retinal development by determining the changes in the expression patterns of their receptors during development of the normal rat retina. METHODS: The expression of type I and type II receptors of the TGF-beta superfamily was observed at the protein level in rat eyes at embryonic age 17 days (E17), at birth (P0), at postnatal days 3, 6, 9, and at 11 weeks (P3, P6, P9, and adult, respectively). RESULTS: Activin type I receptor and BMP type IB receptor were first detected in P6 and P3 retinas, respectively, at the protein level, and activin type II receptor was first detected in the P0 retina. The other receptors (TGF-beta type I and II receptors, activin type IB receptor, BMP types IA and II receptors) were detected at E17. The period from P0 to P9 corresponded to the period of dynamic changes in the rat retinal development. CONCLUSION: The results suggest that the expression of TGF-beta superfamily is regulated along with retinal development and may be related to retinal development.

Activin Receptors, Type I↗
PubMed2003

Vascular endothelial growth factor-B and retinal vascular development in the mouse.

PURPOSE: Vascular endothelial growth factor-A (VEGF-A) is crucial to retinal vascular growth, both normal and pathological. VEGF-B, recently characterized, is reported to be expressed in retinal tissues, but the importance of VEGF-B to retinal vascular development remained unknown. The aim of this study was to analyse retinal vascular growth in the Vegfb-/- knockout mouse. METHODS: Retinal vascular growth was measured in Vegfb-/- knockout mice raised under normal conditions, and Vegfb-/- knockout mice with an oxygen-induced proliferative retinopathy. Wild type Vegfb+/+ mice served as controls. Vessels were perfused with ink and retinal flatmounts secondarily labelled with FITC-lectin (BS-1, Griffonia simplicifolia). Area and diameter of retinal growth and retinal vascular growth were recorded over days 0-20, and capillary density and mean diameter recorded from day 17 pups. RESULTS: A variety of techniques confirmed that Vegfb+/+ mice expressed VEGF-B and that VEGF-B expression was absent in Vegfb-/- mice. Vegfb-/- mice raised in room air showed no significant differences from Vegfb+/+ controls. No differences were found in oxygen-induced retinopathy between Vegfb-/- and Vegfb+/+ pups in either the extent of the initial oxygen-induced ablation, or in the regrowth of retinal vessels or vitreal (neovascular) sprouts; vitreal sprouts are important markers of the abnormal proliferative response, and are maximally expressed on day 17 in this model of oxygen-induced retinopathy. CONCLUSIONS: These results indicate that a lack of VEGF-B does not significantly affect development of the retinal vasculature under normal conditions, nor does it appear to affect the proliferative retinal responses seen in oxygen-induced retinopathy.

Animals↗
PubMed1998

Role of retinal vascular endothelial cells in development of CMV retinitis.

PURPOSE: Although cytomegalovirus (CMV) retinitis is known to occur in association with retinal microangiopathy in individuals with marked immunodeficiency, glial cells are believed to be the initial target cells in the development of retinitis. Moreover, it has been hypothesized that CMV gains access to the retinal glia because of altered vascular permeability. In an attempt to address the hypothesis, we studied 30 autopsy eyes of AIDS patients with systemic CMV infection, with or without clinically apparent CMV retinitis. METHODS: The autopsy eyes were processed in three ways. First, dual immunohistochemical studies were done by using anti-CMV antibodies for immediate early, early, and late antigens. The retinal cell types infected with the virus were then determined by using anti-GFAP, anti-VonWillebrand's factor, neuronal specific enolase, and leukocyte marker CD68. Second, selected eyes were processed for in situ hybridization with DNA probe specific to CMV. Third, an eye with clinically apparent CMV retinitis was submitted for electron microscopic examination. RESULTS: At the site of retinal necrosis in those eyes with a clinical diagnosis of CMV retinitis, the immunohistochemical, in situ hybridization, and ultrastructural examinations revealed that CMV was present primarily in the Müller cells and in perivascular glial cells. Adjacent to these infected cells, focal areas of positive staining for CMV antigen were seen in the glial cells, neuronal cells, and retinal pigment epithelial cells. At these sites most of the retinal capillaries were devoid of endothelial cells. Few vessels located at the advancing margin of retinal necrosis showed the presence of viral proteins in the endothelial cells. CONCLUSIONS: The present results indicate that retinal vascular endothelial cells could be the initial target in the development of viral retinitis, with subsequent spread of the infection to perivascular glia, Müller cells, and other retinal cells, including the retinal pigment epithelium.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Integrin alpha 2 beta 1 mediates interactions between developing embryonic retinal cells and collagen.

In the developing nervous system, the extracellular matrix provides a source of extrinsic cues to guide determination of cell fate, neuroblast migration, axon outgrowth and synapse formation. In the neural retina, undifferentiated neuroepithelial precursor cells contact extracellular matrix that contains multiple collagen types. Collagens have been shown to support retinal cell adhesion and neurite outgrowth, but the integrin receptors mediating neuronal responses are not understood. Here we provide evidence that integrin alpha 2 beta 1 acts as a collagen receptor in the developing avian retina and examine its expression pattern. Using a recently described monoclonal antibody, MEP-17, alpha 2 protein was detected in the developing retina by immunofluorescence in tissue sections and dissociated cells, and by immunoprecipitation. At embryonic day 4 (E4), when the majority of retinal cells are undifferentiated neuroepithelial cells, alpha 2 immunoreactivity in sections was widespread and about half of cells dissociated in culture were alpha 2 positive. At E6, after the retinal ganglion cell layer had differentiated, immunoreactivity in sections decreased in the central, more developed portion of the retina and 25% of dissociated cells were alpha 2 positive. E6 retinal ganglion cells, identified by neurofilament immunoreactivity, did not express detectable alpha 2 immunoreactivity. Immunoprecipitation experiments using E6 extracts demonstrated that the alpha 2 subunit was paired with the beta 1 integrin subunit. By E12, alpha 2 immunoreactivity in sections was confined to the extreme peripheral retina, although the antigen may be masked since expression levels comparable to or slightly higher than E6 could be detected in dissociated cells and extracts. By employing function blocking antibodies, it was shown that alpha 2 beta 1 integrin is necessary for cell adhesion and process outgrowth by embryonic retinal cells on collagens I and IV. Although alpha 2 expression continued through E12, alpha 2 activity was down regulated with increasing embryonic age, since alpha 2-dependent adhesion and outgrowth declined. These data suggest a role for alpha 2 beta 1 in neuroepithelial cell interactions with collagen rather than for axon extension by retinal ganglion cells.

Animals↗
PubMed2001

EMAP cytokine expression in developing retinas of normal and retinal degeneration (rd) mutant mice.

Endothelial-monocyte-activating polypeptide (EMAP) is a proinflammatory cytokine and a mediator of programmed endothelial cell death. To gain insight into its possible functions during retinal development and degeneration, the cellular distribution of EMAP protein was compared in control and retinal degeneration (rd) mice. EMAP immunoreactivity was confined to the ganglion cell layer (GCL) and the inner nuclear layer (INL). There were significant differences in the intensity of EMAP labeling in the GCL and the INL when comparing control and rd mouse retinas. Rd retinas contain much more EMAP immunoreactivity in the GCL and the INL than the control retinas at postnatal day 14, which is the time point immediately after the onset of the degeneration of the rd retina. Histopathologic examination showed no significant abnormalities in the GCL and INL in the rd mouse, despite a great degree of photoreceptor cell death from P12 to P18. Light and electron microscopic studies immunolocalize EMAP protein to the cytoplasm of retinal ganglion cells, amacrine cells, and horizontal cells. The data suggests that EMAP is synthesized and accumulated as an intracellular precursor protein that has a functional role in translation and protein synthesis as a cofactor for tRNA synthetase. The increased expression of EMAP precursor levels in rd mouse retina may reflect the enhanced rate of translation and protein synthesis in the production of endogenous factors that promote survival in the GCL and INL.

Animals↗
PubMed2002

[Transcription changes of alpha A-crystallins gene during the development of retinal degeneration in Rd, Rds and C3H mouse].

PURPOSE: To determine the relationship between retinal alpha A-crystallins and the development of retinal degeneration in rd, rds and C3H mice. METHODS: Total retinal mRNA was prepared from the retina of (rd) retinal degeneration, (rds) retinal degeneration slow, C3H and control C3B mice during the progress of retinal degeneration (Post-natal 3, 4, 5, 6, 8 weeks). The retinal expression of alpha A-crystallins was determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis. RESULTS: Expression of retinal alpha A-crystallins is rather stable in rd, rds and C3H mice during the progress of their retinal degeneration. The expression is also similar to that in normal C3B mice but different to that in Royal college of surgeons(RCS) rats. CONCLUSION: Retinal alpha A-crystallins may not involve in the course of RP in rd, rds and C3H mice. The molecular mechanism of RP in rd, rds and C3H may be different to that in RCS rat.

Animals↗
PubMed2016

Substituting mouse transcription factor Pou4f2 with a sea urchin orthologue restores retinal ganglion cell development.

Pou domain transcription factor Pou4f2 is essential for the development of retinal ganglion cells (RGCs) in the vertebrate retina. A distant orthologue of Pou4f2 exists in the genome of the sea urchin (class Echinoidea) Strongylocentrotus purpuratus (SpPou4f1/2), yet the photosensory structure of sea urchins is strikingly different from that of the mammalian retina. Sea urchins have no obvious eyes, but have photoreceptors clustered around their tube feet disc. The mechanisms that are associated with the development and function of photoreception in sea urchins are largely unexplored. As an initial approach to better understand the sea urchin photosensory structure and relate it to the mammalian retina, we asked whether SpPou4f1/2 could support RGC development in the absence of Pou4f2. To answer this question, we replaced genomic Pou4f2 with an SpPou4f1/2 cDNA. In Pou4f2-null mice, retinas expressing SpPou4f1/2 were outwardly identical to those of wild-type mice. SpPou4f1/2 retinas exhibited dark-adapted electroretinogram scotopic threshold responses, indicating functionally active RGCs. During retinal development, SpPou4f1/2 activated RGC-specific genes and in S. purpuratus, SpPou4f2 was expressed in photoreceptor cells of tube feet in a pattern distinct from Opsin4 and Pax6. Our results suggest that SpPou4f1/2 and Pou4f2 share conserved components of a gene network for photosensory development and they maintain their conserved intrinsic functions despite vast morphological differences in mouse and sea urchin photosensory structures.

Animals↗
PubMed1991

[Retinal detachment after perforating eye injuries. II. The interval between injury and retinal detachment and factors which may have contributed to the development of retinal detachment].

The authors operated in 1977-1987 by the cryosurgical method 69 patients after injuries on account of detachment of the retina. Detachment developed in 37 patients after simple perforation of the eye and in 32 patients after perforation of the eye with a foreign intraocular body. In all patients the perforation reached as far as the vitreous body. The interval injury--detachment was assessed retrospectively. The authors found that for the development of post-traumatic detachment of the retina a period of two years after the injury is decisive--within this period detachment of the retina occurred in 55% of the cases. Another 31.9% of the cases occurred during the late post-traumatic period, i.e. 6-40 years after injury. In 21.7% patients anamnestic data were found which were, no doubt, associated with the detachment of the retina: surgical trauma in 8.7%, direct contusion of the eye in 10.1% and lifting a heavy burden in 2.9%.

Adolescent↗
PubMed1995

Immune predispositions for cytomegalovirus retinitis in AIDS. The HNRC Group.

CMV retinitis develops in approximately 28-35% of all AIDS patients at later stages of disease, often leading to blindness. To determine whether the subset of AIDS patients who developed CMV retinitis (CMV-R) were immunologically predisposed, T cell proliferation responses to CMV were examined prospectively in an HIV infected, HLA typed, longitudinal study population. Individuals who developed CMV-R had significantly lower T cell proliferation responses to CMV, both early and late in disease, compared to CD4 matched controls who have not developed CMV-R. Since HLA proteins influence T-cell recognition, phenotypes of 21 CMV-R patients were examined to determine whether certain HLA alleles were associated with low immune response and predisposed AIDS patients to CMV-R. HLA DR7 and B44 were at increased (nearly twice the expected) frequency in those with CMV-R. The combined association of either B44, 51 or DR7 with CMV-R was highly significant (P = .008, relative risk of CMV-R = 15) with correction for multiple comparisons. Low immune responses were twice as frequent in those with (61%) compared to those without (30%) predisposing alleles. Thus, AIDS patients with immunogenetically related hyporesponsiveness to CMV antigens may be at increased risk of retinitis.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Role of hypoxia during normal retinal vessel development and in experimental retinopathy of prematurity.

PURPOSE: To test the hypothesis that retinal hypoxia is present during vascular development in normal rat pups and in a newborn rat model of retinopathy of prematurity (ROP). METHODS: Preretinal vitreous PO(2) measurements were made during room air breathing using (19)F magnetic resonance spectroscopy (MRS) and a perfluoro-15-crown-5-ether droplet in normal adult and newborn (postnatal day [P]1-P20) rats, and in newborn rats exposed first to 14 days of variable oxygen (before NV) and six additional days in room air after variable oxygen exposure (during NV). After each experiment, blood gas values were measured, and retinas were isolated. Retinas were adenosine diphosphatase (ADPase) stained, and flatmounted to determine peripheral avascular extent and NV incidence and severity. RESULTS: In the vascularized rat retina, no significant difference (P > 0.05) was found between the droplet-derived preretinal vitreous oxygen tension (24 +/- 2 mm Hg, mean +/- SEM, n = 18) and previously reported electrode-measured oxygen tension (22 +/- 1 mm Hg). Only during normal retinal vessel growth (P1-P10) and before the appearance of NV was evidence for retinal hypoxia found at the border of the vascular and avascular retina. However, the mean PO(2) (range, 24-28 mm Hg) over the vascular retina was not different (P > 0.05) between any of the newborn rat groups in this study. CONCLUSIONS: (19)F MRS of a perfluorocarbon droplet provides an accurate measure of preretinal vitreous oxygen tension in rats. These data support an important role of physiologic hypoxia in normal retinal circulatory development and raises the possibility that, in experimental ROP, retinal hypoxia is a necessary but not sufficient condition for the development of retinal NV.

Animals↗
PubMed2003

The receptor protein tyrosine phosphatase mu, PTPmu, regulates histogenesis of the chick retina.

The formation of laminae within the retina requires the coordinate regulation of cell differentiation and migration. The cell adhesion molecule and member of the immunoglobulin superfamily, receptor protein tyrosine phosphatase Mu, PTPmu, is expressed in precursor and early, differentiated cells of the prelaminated retina, and later becomes restricted to the inner plexiform, ganglion cell, and optic fiber layers. Since the timing of PTPmu expression correlates with the peak period of retinal lamination, we examined whether this RPTP could be regulating cell adhesion and migration within the retina, and thus influencing retinal development. Chick retinal organ cultures were infected with herpes simplex viruses encoding either an antisense sequence to PTPmu, wild-type PTPmu, or a catalytically inactive mutant form of PTPmu, and homophilic adhesion was blocked by using a function-blocking antibody. All conditions that perturbed PTPmu dramatically disrupted retinal histogenesis. Our findings demonstrate that catalytic activity and adhesion mediated by PTPmu regulate lamination of the retina, emphasizing the importance of adhesion and signaling via receptor protein tyrosine phosphatases in the developing nervous system. To our knowledge, this is the first demonstration that an Ig superfamily RPTP regulates the lamination of any neural tissue.

Animals↗
PubMed1989

[Acute necrotizing retinitis following varicella zoster virus infection].

As far as we know today, acute retinal necrosis is caused by infection with a virus of the herpes group. Reports are occasionally published of retinitis developing before or after herpes zoster dermatitis. The present paper reports the case of a patient who developed a retinitis of the right eye five years after a herpes zoster infection of the ophthalmic nerve. Studies and treatment of VZV retinitis and retinitis before or after zoster retinitis reported in the literature are summarized. The possible mechanisms of generalization (neurogenic or hematogenous) are analyzed.

Acute Disease↗
PubMed2000

The conditional medaka mutation eyeless uncouples patterning and morphogenesis of the eye.

In early vertebrate eye development, the retinal anlage is specified in the anterior neuroectoderm. During neurulation, the optic vesicles evaginate from the lateral wall of the prosencephalon. Here we describe the temperature-sensitive mutation eyeless in the Japanese medakafish. Marker gene analysis indicates that, whereas, specification of two retinal primordia and proximodistal patterning takes place in the mutant embryo, optic vesicle evagination does not occur and subsequent differentiation of the retinal primordia is not observed. The mutation eyeless thus uncouples patterning and morphogenesis at early steps of retinal development. Temperature-shift experiments indicate a requirement for eyeless activity prior to optic vesicle evagination. Cell transplantation shows that eyeless acts cell autonomously.

Animals↗
PubMed2003

Postnatal serum insulin-like growth factor I deficiency is associated with retinopathy of prematurity and other complications of premature birth.

OBJECTIVE: Insulin-like growth factor I (IGF-I) is necessary for normal development of retinal blood vessels in mice and humans. Because retinopathy of prematurity (ROP) is initiated by abnormal postnatal retinal development, we hypothesized that prolonged low IGF-I in premature infants might be a risk factor for ROP. DESIGN: We conducted a prospective, longitudinal study measuring serum IGF-I concentrations weekly in 84 premature infants from birth (postmenstrual ages: 24-32 weeks) until discharge from the hospital. Infants were evaluated for ROP and other morbidity of prematurity: bronchopulmonary dysplasia (BPD), intraventricular hemorrhage (IVH), and necrotizing enterocolitis (NEC). RESULTS: Low serum IGF-I values correlated with later development of ROP. The mean IGF-I +/- SEM level during postmenstrual ages 30-33 weeks was lowest with severe ROP (25 +/- 2.41 micro g/L), 29 +/- 1.76 micro g/L with moderate ROP, and 33 +/- 1.72 micro g/L with no ROP. The duration of low IGF-I also correlated strongly with the severity of ROP. The interval from birth until serum IGF-I levels reached >33 micro g/L was 23 +/- 2.6 days for no ROP, 44 +/- 4.8 days for moderate ROP, and 52 +/- 7.5 days for severe ROP. Each adjusted stepwise increase of 5 micro g/L in mean IGF-I during postmenstrual ages 30 to 33 weeks decreased the risk of proliferative ROP by 45%. Other complications (NEC, BPD, IVH) were correlated with ROP and with low IGF-I levels. The relative risk for any morbidity (ROP, BPD, IVH, or NEC) was increased 2.2-fold (95% confidence interval: 1.41-3.43) if IGF-I was <or=33 micro g/L at 33 weeks' postmenstrual age. CONCLUSIONS: These results indicate that persistent low serum concentrations of IGF-I after premature birth are associated with later development of ROP and other complications of prematurity. IGF-I is at least as strong a determinant of risk for ROP as postmenstrual age at birth and birth weight.

Birth Weight↗
PubMed2006

Photoreceptor cell apoptosis in the retinal degeneration of Uchl3-deficient mice.

UCH-L3 belongs to the ubiquitin C-terminal hydrolase family that deubiquitinates ubiquitin-protein conjugates in the ubiquitin-proteasome system. A murine Uchl3 deletion mutant displays retinal degeneration, muscular degeneration, and mild growth retardation. To elucidate the function of UCH-L3, we investigated histopathological changes and expression of apoptosis- and oxidative stress-related proteins during retinal degeneration. In the normal retina, UCH-L3 was enriched in the photoreceptor inner segment that contains abundant mitochondria. Although the retina of Uchl3-deficient mice showed no significant morphological abnormalities during retinal development, prominent retinal degeneration became manifested after 3 weeks of age associated with photoreceptor cell apoptosis. Ultrastructurally, a decreased area of mitochondrial cristae and vacuolar changes were observed in the degenerated inner segment. Increased immunoreactivities for manganese superoxide dismutase, cytochrome c oxidase I, and apoptosis-inducing factor in the inner segment indicated mitochondrial oxidative stress. Expression of cytochrome c, caspase-1, and cleaved caspase-3 did not differ between wild-type and mutant mice; however, immunoreactivity for endonuclease G was found in the photoreceptor nuclei in the mutant retina. Hence, loss of UCH-L3 leads to mitochondrial oxidative stress-related photoreceptor cell apoptosis in a caspase-independent manner. Thus, Uchl3-deficient mice represent a model for adult-onset retinal degeneration associated with mitochondrial impairment.

Animals↗
PubMed1990

Borna disease virus-induced retinitis in Lewis rats--an immune-mediated retinopathy.

Borna disease virus (BDV) infection, naturally occurring in horses and sheep induces a mononuclear retinitis and meningoencephalitis in adult Lewis rats. In the pathogenesis a virus-specific cell mediated immune reaction presumably of delayed hypersensitivity type is operative. Corresponding to the encephalitic lesions a progressive retinitis with loss of the first and second retinal neuron develops. The inflammatory response is characterized by predominance of macrophages in the early phase of infection followed by distinct plasmacellular infiltration. Immunosuppressed and immuno-incompetent rats do not develop retinal lesions after intracerebral inoculation. Thus similar as in the brain probably virus specific immunopathological reactions play a crucial role in the pathogenesis of BDV-induced retinitis in Lewis rats.

Animals↗