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At least 487 records · Page 27Linked to original sources
PubMed2004

Smad3 is required for dedifferentiation of retinal pigment epithelium following retinal detachment in mice.

Retinal pigment epithelial (RPE) cells dedifferentiate and undergo epithelial-mesenchymal transition (EMT) following retinal detachment, playing a central role in formation of fibrous tissue on the detached retina and vitreous retraction (proliferative vitreoretinopathy (PVR)). We have developed a mouse model of subretinal fibrosis with implications for PVR in which retinal detachment is induced without direct damage to the RPE cells. Transforming growth factor-beta (TGF-beta) has long been implicated both in EMT of RPEs and the development of PVR. Using mice null for Smad3, a key signaling intermediate downstream of TGF-beta and activin receptors, we show that Smad3 is essential for EMT of RPE cells induced by retinal detachment. De novo accumulation of fibrous tissue derived from multilayered RPE cells was seen following experimental retinal detachment in eyes of wild type, but not Smad3-null mice. Expression of alpha-smooth muscle actin, a hallmark of EMT in this cell type, and extracellular matrix components, lumican and collagen VI, were also not observed in eyes of Smad3-null mice. Our data show that induction of PDGF-BB by Smad3-dependent TGF-beta signaling is likely an important secondary proliferative component of the disease process. The results suggest that blocking the Smad3 pathway might be beneficial in prevention/treatment of PVR.

Actins↗
PubMed2005

Foveal detachment after successful retinal reattachment for macula on rhegmatogeneous retinal detachment: an ocular coherence tomography evaluation.

PURPOSE: Foveal detachment after apparently successful retinal reattachment surgery for macula-on retinal detachments (RDs) has been previously documented. This pilot study aimed to utilize ocular coherence tomography (OCT) imaging to investigate foveal architecture after routine retinal detachment surgery and correlate this to visual acuity. METHODS: Prospective recruitment of patients attending one unit with macula-on RDs. Patients underwent full clinical examination including OCT preoperatively and RD surgery undertaken by scleral buckling, external drainage and air injection. Postoperatively patients had clinical examinations and OCT at 1 week, 1, 3, 6, and 12 months. RESULTS: A total of 12 consecutive patients were recruited into the study. All had macula-on RDs and normal OCTs at onset. There were no operative or postoperative complications. Retinal reattachment was achieved in all cases within 24 h postoperatively. At 1 month six of 12 patients (50%) showed foveal detachment on OCT, which was invisible on clinical examination. At 3 months, the foveal detachment persisted in four (33%) of these patients. In these cases the foveal detachment persisted at 6 months follow-up, however, a reduction in subfoveal fluid was noted. All cases had foveal reattachment by 12 months postoperatively. Visual acuity was closely correlated to the presence of foveal attachment. DISCUSSION: A high proportion of patients with successful retinal reattachment surgery had foveal detachments postoperatively. This phenomenon was associated with reduced visual acuity. The aetiology of this occurrence is unknown and warrants further investigation as there is the potential of a long-term effect on vision.

Adult↗
PubMed2006

Bilateral giant retinal tear and retinal detachment in a young emmetropic man after Jarish-Herxheimer reaction in ocular syphilis.

BACKGROUND: Giant retinal tears were previously described in patients affected by panuveitis. We report the case of a patient presenting giant retinal tears in both eyes affected by ocular syphilis. PATIENT AND METHOD: A 45-year-old patient presented a 5 days history of sudden bilateral drop of vision, two weeks after penicillin therapy for secondary syphilis. The best visual acuity was 0.5 RE and light perception LE. Biomicroscopy showed an intense vitritis associated with bilateral giant tear and retinal detachment. Both TPHA and VDRL were positive. Lumbar puncture showed lymphoplasmocytosis with intrathecal synthesis of IgM. RESULTS: Topical steroids treatment was applied and intravenous penicillin was given during 14 days. Pars plana vitrectomy with silicon oil tamponade was performed in association with endophotocoagulation in the left eye and cryocoagulation in the right eye. Vitreous PCR was negative. Evolution was successful with an attached retina. CONCLUSIONS: This represents the first reported case of giant retinal tear with retinal detachment in a patient presenting a syphilitic panuveitis.

Humans↗
PubMed2002

Naturally occurring rhodopsin mutation in the dog causes retinal dysfunction and degeneration mimicking human dominant retinitis pigmentosa.

Rhodopsin is the G protein-coupled receptor that is activated by light and initiates the transduction cascade leading to night (rod) vision. Naturally occurring pathogenic rhodopsin (RHO) mutations have been previously identified only in humans and are a common cause of dominantly inherited blindness from retinal degeneration. We identified English Mastiff dogs with a naturally occurring dominant retinal degeneration and determined the cause to be a point mutation in the RHO gene (Thr4Arg). Dogs with this mutant allele manifest a retinal phenotype that closely mimics that in humans with RHO mutations. The phenotypic features shared by dog and man include a dramatically slowed time course of recovery of rod photoreceptor function after light exposure and a distinctive topographic pattern to the retinal degeneration. The canine disease offers opportunities to explore the basis of prolonged photoreceptor recovery after light in RHO mutations and determine whether there are links between the dysfunction and apoptotic retinal cell death. The RHO mutant dog also becomes the large animal needed for preclinical trials of therapies for a major subset of human retinopathies.

Animals↗
PubMed2001

Immune response to retinal antigens in patients with gyrate atrophy and other hereditary retinal dystrophies.

PURPOSE: Gyrate atrophy (GA) is a rare hereditary disease that causes retinal destruction. Retinal damage in GA and other heredodegenerative diseases such as retinitis pigmentosa (RP) releases sequestered antigens and may trigger immune response to these molecules. Here, we studied the immune response to retinal antigens in patients with GA and RP and compared it with that of patients with inactive posterior uveitis and normal volunteers. PATIENTS AND METHODS: Peripheral blood was collected from 24 patients with RP, 10 patients with GA, 10 patients with inactive posterior uveitis, and 16 normal volunteers. Cell-mediated immune responses to human S-antigen (HS-Ag), bovine S-antigen (BS-Ag), and interphotoreceptor retinoid-binding protein (IRBP) were investigated by lymphocyte proliferation assay. In addition, serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were studied by ELISA. Immunologic data were correlated with clinical and electrophysiological findings. RESULTS: Patients with GA or RP responded to HS-Ag and BS-Ag more vigorously than patients with uveitis or healthy controls, as shown by higher mean stimulation indices and larger proportions of responders. Unlike S-Ag, IRBP stimulated low lymphocyte responses in only a small proportion of RP patients. The mean sVCAM-1 levels were significantly higher in the sera from patients with GA than in that from normal controls. CONCLUSION: An elevated cellular immune response to S-Ag is common in patients with GA and RP. This elevated cellular immune response to S-Ag may exacerbate retinal destruction in patients with GA and RP.

Adolescent↗
PubMed2004

Correlation of retinal function with retinal histopathology following ischemia-reperfusion in rat eyes.

PURPOSE: To investigate the relationship between retinal function and histopathology following retinal ischemia-reperfusion in rats. METHODS: Retinal ischemia was induced in 27 Sprague-Dawley rats by raising the intraocular pressure for 60- or 90-minutes. Two weeks after the retinal ischemia-reperfusion, ganzfeld stimuli of different luminances (maximum 0.51 log cd-s/m2) were used to elicit full-field ERGs from the right (experimental) and left (control) eyes. The amplitudes of the scotopic b-waves were measured, and intensity-response curves were plotted. The b-wave amplitudes at the initial peak (VbIP), the dip (Vb(dip)), and the maximum stimulus intensity (Vb(max)) were measured. The animals were sacrificed after the ERG recordings to determine the surviving retinal cells in the inner nuclear layer (INL). RESULTS: The log values of the VbIP, Vb(dip) and Vb(max) were linearly correlated with the number of surviving cells in the INL (r = 0.928, 0.905, and 0.913 for VbIP, Vb(dip) and Vb(max), respectively; p < 0.0001 for each). The slope of the regression line for the Vb(dip) was significantly steeper than that for the VbIP and Vb(max) (p < 0.005). The regression line for the Vb(dip) reached undetectable level of the b-wave (<1 microV) even though approximately 25% of the cells still remained in the INL. CONCLUSIONS: The amplitude of the scotopic b-wave is a sensitive index of the surviving INL cells. However, if one selects the stimulus intensity at the dip, the functional loss would be exaggerated in spite of the presence of cells in the INL.

Animals↗
PubMed1998

Cytomegalovirus retinitis and viral resistance: ganciclovir resistance. CMV Retinitis and Viral Resistance Study Group.

Cytomegalovirus (CMV) retinitis is among the most common opportunistic infections in patients with AIDS and a substantial cause of visual loss. With long-term therapy, resistant CMV may develop. In a prospective study of 108 patients with CMV retinitis, 80.6% of patients were found to have either a positive blood culture or positive urine culture for CMV at the diagnosis of retinitis. At diagnosis of retinitis, 0.9% and 2.7% of patients had a ganciclovir-resistant blood culture isolate and urine culture isolate, respectively. Of 76 patients initially treated with ganciclovir, 11.4% had a resistant blood or urine culture isolate by 6 months of treatment and 27.5% by 9 months. The development of ganciclovir resistance during follow-up correlated with the occurrence of CMV retinitis in the contralateral eye (odds ratio = 9.06, P = .003).

AIDS-Related Opportunistic Infections↗
PubMed2006

Human retinal and brain cell lines: A model of HCMV retinitis and encephalitis.

Although HIV is accepted as the etiologic agent in AIDS, other factors have been implicated in accelerating the disease. Human cytomegalovirus (HCMV) in particular has been implicated as a cofactor in the progression from AIDS-related complex (ARC) to AIDS. HCMV infection of the central nervous system (CNS) (brain, retina) has been reported in at least 50% of AIDS patients, and has been implicated in producing encephalitis and sight-threatening retinitis. HCMV exhibits strict species specificity and animal models for human HCMV are conspicuous by their absence. We have developed a human brain cell line (mixed glial/neuronal) and a multipotential human retinal precursor cell line (neuronal in nature). We have tested the suitability of these cell lines as models for the study of HCMV infectibility. In this study, we report that these cell lines are optimal for the study of HCMV infectibility and pathogenesis in tissues of neural origin and appropriate to study HIV-HCMV interaction. Immortalized human brain and retinal cell lines were infected with a laboratory strain of HCMV (AD 169, Towne) at a multiplicity of infection moi (1-5) and viral infectibility and cell specificity monitored by: (a) phenotypic analysis (multinucleate cells, syncytium formation, etc.), (b) antigen expression (IE, E, late) by immunohistochemistry, Western blot analysis, (c) presence of viral particles by TEM, and (d) expression of indicator plasmids (HIV-LTR-CAT). We report that both human retinal and brain cell lines are permissive for HCMV infectibility. Cell specificity was not seen; both cells expressing glial/neuronal cell markers were positive for the presence of HCMV early/late antigens. Formation of multinucleate giant cells with nuclear inclusion bodies and syncytia were seen. Productive viral infection was confirmed by the ability of cell-free supernatant from the third passage of infected cells to produce pathogenicity and express viral particles, when added to fresh cultures. Using indicator plasmids, HIV-LTR, and CAT, we have shown that HIV and HCMV interact at the cellular level. We have also shown that HIV production in retinal and brain cell lines transfected with cloned HIV was enhanced by HCMV-IE genes. We did not see any differences in HCMV. AD 169, Towne isolate, and data from both strains is presented in this paper. This model could prove extremely useful for the study of cell specificity/cellular and molecular interaction between HIV/HCMV and to test antiviral therapies.

Animals↗
PubMed1993

Effects of dopamine antagonists on retinal B-wave recovery after retinal ischemia.

Retinal ischemia was developed by occlusion of the central retinal artery for 30 minutes. The artery was reperfused thereafter, and the recovery of the b-wave amplitude was determined as an indication of the recovery of retinal function after ischemia. Following ischemia, it was found that dopamine antagonists, including chlofluperol, metoclopramide, trifluperol and droperidol, increased in b-wave amplitude recovery significantly over the control b-wave recovery. Similar effects were observed with haloperidol and loxapine, but to a lesser extent. The results correlated well with the improvement of retinal blood flow by these dopamine antagonists (4,5). Neither floropipamide, a dopamine antagonist, nor bromocriptine, a dopamine agonist, affected the b-wave recovery after ischemia. These results also correlate well with the inability of these agents to increase the retinal blood flow measured by the microsphere technique (4,5). These findings suggest that most of the dopamine antagonists, with the exception of floropipamide, could be used for the treatment and/or prevention of ischemic retinopathy.

Animals↗
PubMed2006

Muller glia induce retinal progenitor cells to differentiate into retinal ganglion cells.

Retinal progenitor cells could differentiate into various retinal cells that made cell-replacement therapy possible. Here, we investigated the role of cellular microenvironment on their regulation and differentiation and found that the percentage of proliferating cells and the percentage of retinal ganglion cells produced from them increased, when retinal progenitor cells were cocultured with Muller glia. Muller glia conditioned medium had the similar results. It is speculated that rather than traditional supportive roles, Muller glia may have an active regulatory role inducing retinal progenitor cells to proliferate and differentiate into ganglion cells by secreting some diffusible and membrane-associated factors. Identification of Muller glia-derived factors will be made to elucidate the molecular mechanisms of neurogenesis.

Animals↗
PubMed1993

Trophic factors produced by retinal cells increase the survival of retinal ganglion cells in vitro.

The naturally occurring neuron death of normal development has been shown to depend on trophic factors produced and released by target cells. It has also been shown that the afferent supply and local interactions play a role in the control of this degenerative phenomenon. We studied the effect of trophic factors produced by intrinsic retinal cells on the survival of retinal ganglion cells in vitro. Retinae of newborn hooded rats were retrogradely labelled with horseradish peroxidase injected into the superior colliculus to permit the identification of retinal ganglion cells in culture. We tested the effect of conditioned media either from aggregates or from explants of retinal cells from neonatal rats on the survival of ganglion cells in vitro. Our results showed that both conditioned media increased the survival of these cells. The trophic activity was dose-dependent, was maintained after dialysis against a 12 kDa membrane, was abolished by heating at 56 degrees C for 30 min, and was not found in conditioned medium from cerebral cortical explants. Conditioned medium obtained without fetal calf serum presented the same trophic effect. These results suggest that the local control of developmental neuron death by intrinsic retinal cells may be mediated by neurotrophic factors.

Animals↗
PubMed2005

Relation of pre-LASIK and post-LASIK retinal lesions and retinal examination for LASIK eyes.

AIMS: Analysis of highly myopic eyes (mean myopia -11 D) with post-LASIK vitreoretinal complications (breaks, retinal detachment) that also had pre-LASIK vitreoretinal pathology (lattice, breaks). METHODS: Retrospective case series. RESULTS: 67 eyes in 56 patients with pre-LASIK retinal examination developed post-LASIK vitreoretinal complications. 17 of the 67 eyes (25.4%) had pre-LASIK vitreoretinal pathology. 10 of the 17 eyes that underwent pre-LASIK prophylactic retinal treatment still developed post-LASIK lesions. They developed adjacent to pre-LASIK lesions for 15 of 17 eyes (88.2%), and outside of quadrant(s) of pre-LASIK lesions for five eyes (29.4%). CONCLUSION: Pre-LASIK retinal examination may predict locations of certain post-LASIK retinal lesions that may develop in highly myopic eyes with pre-LASIK vitreoretinal pathology, but prophylactic treatment may not prevent all post-LASIK vitreoretinal complications.

Adult↗
PubMed1999

Modulating phenotype and cytokine production of leucocytic retinal infiltrate in experimental autoimmune uveoretinitis following intranasal tolerance induction with retinal antigens.

BACKGROUND/AIM: Nasal administration of retinal antigens induces systemic tolerance which results in suppression of experimental autoimmune uveoretinitis (EAU) when subsequently exposed to antigen. The aim was to establish if tolerance induction alters retinal infiltrating leucocyte phenotype and cytokine profile in tolerised animals when there is significantly reduced tissue destruction despite immunisation with retinal antigen. METHODS: Female Lewis rats were tolerised by intranasal administration with retinal extract (RE) before immunisation with RE to induce EAU. Control animals were administered phosphate buffered saline (PBS) intranasally. Post immunisation, daily clinical responses were recorded and at the height of disease, retinas were removed and either infiltrating leucocytes isolated for flow cytometric phenotype assessment and intracellular cytokine production, or chorioretina processed for immunohistochemistry. Fellow eyes were assessed for cytokine mRNA by semiquantitative RT-PCR. RESULTS: Flow cytometric analysis showed that before clinical onset of EAU there is no evidence of macrophage infiltration and no significant difference in circulating T cell populations within the retina. By day 14 a reduced retinal infiltrate in tolerised animals was observed and in particular a reduction in numbers of "activated" (with respect to CD4 and MHC class II expression) macrophages. Immunohistochemistry confirmed these findings and additionally minimal rod outer segment destruction was observed histologically. Cytokine analysis revealed that both IL-10 mRNA and intracellular IL-10 production was increased in tolerised eyes 7 days post immunisation. Although by day 14 post immunisation, IL-10 production was equivalent in both groups, a reduced percentage of IFN-gamma + macrophages and IFN-gamma + CD4+ T cells with increased percentage of IL-4+ CD4+ T cells were observed in tolerised animals. CONCLUSIONS: Leucocytic infiltrate is not only reduced in number but its distinct phenotype compared with controls implies a reduced activation status of infiltrating monocyts to accompany increased IL-10 and reduced IFN-gamma production in tolerised animals. This modulation may in turn contribute towards protection against target organ destruction in EAU.

Animals↗
PubMed1984

Retinitis pigmentosa and retinal degeneration in animals: a review.

Recent biochemical findings in the human disease, retinitis pigmentosa, and related retinal degenerative diseases in animals were reviewed and discussed. While the biochemical etiology of the human disease is not known, there are indications that retinal degeneration in the rd mouse and the Irish Setter dog are related to a deficiency in cGMP phosphodiesterase and the accumulation of cGMP in the photoreceptor outer segments. The biochemical basis of retinal degeneration in the Royal College of Surgeons (RCS) rat does not seem to be related to a defect in the metabolism of cGMP, but there are suggestions that a defect in retinoid metabolism may be involved. The possibility that the defect in RCS rats may involve receptors on the membranes of the cells of the retinal pigment epithelium or phagocytic markers on those of the rod outer segment disks was discussed.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMedDate not supplied

Involvement of oxygen free radicals in experimental retinal ischemia and the selective vulnerability of retinal damage.

Protective effects of CV-3611, a free radical scavenger, on retinal ischemic injury in the rat and on glutamate-induced cytotoxicity in a cell line were evaluated. Transient retinal ischemia was induced by raising intraocular pressure of rats to 110 mm Hg for 45 min, and the electroretinogram (ERG) was measured to evaluate retinal function. No ERG could be recorded immediately after reperfusion, and thereafter the ERG gradually recovered. Recovery of the a-wave latency and the amplitudes of the a and b waves in the CV-3611-treated (10 mg/kg, p.o.) group were significantly better than those in the control group up to 24 h after reperfusion. In both the control and CV-3611 group, the b wave showed better recovery than the a wave up to 6 h after reperfusion, while the relationship was reversed after 24-hour reperfusion. Glutamate (10 mM)-induced cytotoxicity in the N18-RE-105 cell, a neural retina-neuroblastoma hybridoma, was quantified by measuring lactate dehydrogenase. Three and 10 microM of CV-3611 significantly attenuated the glutamate-induced cytotoxicity in N18-RE-105 cells. Thus, the radical scavenger (CV-3611) promoted the recovery of retinal function after ischemia-reperfusion injury and ameliorated glutamate-induced cytotoxicity. These results suggest that oxygen free radicals play an important role in the early phase of retinal ischemic injury. Moreover, differential recovery processes of the a and b waves after ischemia suggest that the selective vulnerability of the retina to ischemia could change functionally during the period of reperfusion.

Animals↗
PubMed1985

Ovulatory function and retinal catecholamine concentrations in female rats with and without inherited retinal photoreceptor degeneration.

The timing of the critical period and LH surge during the afternoon of proestrus was unchanged in female rats with degenerated retinal photoreceptors (Hunter and Royal College of Surgeons strains), when compared to female rats with intact retinae (Piebald Virol Glaxo and Wistar strains). Both RCS and Wistar strains responded to constant light (LL) exposure by attaining persistent vaginal cornification at the same rate. In addition, both RCS and Wistar strains regained normal estrous cycles when moved from LL to control lighting (LD). Therefore, an intact retinal photoreceptor layer is not essential for normal ovulatory function. In addition, these results show that the effects of LL on gonadotrophin secretion are mediated through the brain and are not the result of retinal degeneration. Measurements of retinal concentrations of dopamine (DA) and its metabolite, 3,4-dihydroxyphenylacetic acid (Dopac), in Wistar and RCS rats showed that concentrations of both compounds were reduced by LL, and then increased back to control values when animals were moved back into LD. Although the magnitude of the changes in retinal concentrations of DA and Dopac was greater in Wistar than in RCS rats (possibly related to the degeneration which occurs in Wistar but not RCS rats), these results suggest that dopaminergic cells, probably within the amacrine cell population of the retina, respond to different light regimes, perhaps by changes in activity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

Multipotent retinal progenitors express developmental markers, differentiate into retinal neurons, and preserve light-mediated behavior.

PURPOSE: To use progenitor cells isolated from the neural retina for transplantation studies in mice with retinal degeneration. METHODS: Retinal progenitor cells from postnatal day 1 green fluorescent protein-transgenic mice were isolated and characterized. These cells can be expanded greatly in culture and express markers characteristic of neural progenitor cells and/or retinal development. RESULTS: After they were grafted to the degenerating retina of mature mice, a subset of the retinal progenitor cells developed into mature neurons, including presumptive photoreceptors expressing recoverin, rhodopsin, or cone opsin. In rho-/- hosts, there was rescue of cells in the outer nuclear layer (ONL), along with widespread integration of donor cells into the inner retina, and recipient mice showed improved light-mediated behavior compared with control animals. CONCLUSIONS: These findings have implications for the treatment of retinal degeneration, in which neuronal replacement and photoreceptor rescue are major therapeutic goals.

Animals↗
PubMed2006

Hepatocyte growth factor induces retinal vascular permeability via MAP-kinase and PI-3 kinase without altering retinal hemodynamics.

PURPOSE: Although vascular endothelial growth factor (VEGF) is a key mediator of retinal vascular permeability (RVP), there may be additional humoral contributors. Hepatocyte growth factor (HGF) induces endothelial cell separation, regulates expression of cell adhesion molecules and is increased in the vitreous fluid of patients with proliferative diabetic retinopathy. The purpose of this study was to evaluate the in vivo effects of HGF on RVP and retinal hemodynamics and delineate the signaling pathways. METHODS: RVP was assessed by vitreous fluorescein fluorophotometry in rats. Time course and dose-response were determined after intravitreal HGF injection. MAP kinase (MAPK), phosphatidylinositol 3-kinase (PI-3 kinase), and protein kinase C (PKC) involvement were examined by using selective inhibitors. Retinal blood flow (RBF) and mean circulation time (MCT) were evaluated by video fluorescein angiography. RESULTS: HGF increased RVP in a time- and dose-dependent manner. HGF-induced RVP was evident 5 minutes after injection, and reached maximal levels after 25 minutes (+107% versus vehicle, P=0.002). This effect was comparable to that of maximum VEGF stimulation (134%+/-128% at 25 ng/mL). Selective inhibitors of MAPK (PD98059) and PI-3 kinase (LY294002) suppressed HGF-induced RVP by 86%+/-44% (P=0.015) and 97%+/-59% (P=0.021), respectively. Non-isoform-selective inhibition of PKC did not significantly decrease HGF-induced RVP. Although VEGF increases RBF and reduces MCT, HGF did not affect either. CONCLUSIONS: HGF increases RVP in a time- and dose-dependent manner at physiologically relevant concentrations with a magnitude and profile similar to that of VEGF, without affecting retinal hemodynamics. Thus, HGF may represent another clinically significant contributor to retinal edema distinct from the actions of VEGF.

Animals↗