Search results for "Retinal Disorder"

showing 7 items of 17 documents

The Retinal Clock Drives the Expression ofKcnv2, a Channel Essential for Visual Function and Cone Survival

2012

PURPOSE The gene Kcnv2 codes for the voltage-gated potassium channel subunit Kv8.2, which can coassemble with Kv2.1 subfamily members to constitute functional voltage-gated potassium channels. Mutations in the Kcnv2 gene result in a retinal disorder designated "cone dystrophy with supernormal rod response (CDSRR)," revealing that Kcnv2 is essential for visual processing and cone survival. The aim of this study was to determine whether expression of Kcnv2 and Kv2.1 is under circadian regulation and may thus contribute to the clock-driven adjustment of photoreceptor function. METHODS Expression of the genes was recorded in preparations of the whole retina and microdissected retinal neurons by…

MaleRetinal Disordergenetic structuresCell SurvivalCone dystrophy with supernormal rod responseBlotting WesternBiologyReal-Time Polymerase Chain ReactionRetinaRats Sprague-Dawleychemistry.chemical_compoundShab Potassium ChannelsmedicineTranscriptional regulationAnimalsImmunoprecipitationRNA MessengerGeneVision OcularRetinaRetinalAnatomyAdaptation PhysiologicalPotassium channelCircadian RhythmRatsCell biologymedicine.anatomical_structureReal-time polymerase chain reactionGene Expression RegulationchemistryPotassium Channels Voltage-GatedRetinal Cone Photoreceptor CellsFemalesense organsInvestigative Opthalmology & Visual Science
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Intravitreal Docosahexaenoic Acid in a Rabbit Model: Preclinical Safety Assessment

2014

PurposeThe purpose of the present study was to evaluate the retinal toxicity of a single dose of intravitreal docosahexaenoic acid (DHA) in rabbit eyes over a short-term period.MethodsSixteen New Zealand albino rabbits were selected for this pre-clinical study. Six concentrations of DHA (Brudy Laboratories, Barcelona, Spain) were prepared: 10 mg/50 µl, 5 mg/50 µl, 2'5 mg/50 µl, 50 µg/50 µl, 25 µg/50 µl, and 5 µg/50 µl. Each concentration was injected intravitreally in the right eye of two rabbits. As a control, the vehicle solution was injected in one eye of four animals. Retinal safety was studied by slit-lamp examination, and electroretinography. All the rabbits were euthanized one week a…

MaleRetinal degenerationgenetic structuresÀcids grassosPharmacologyBiochemistryMicechemistry.chemical_compoundCorneaMedicine and Health SciencesRatolinsExperimentació animalDegeneració (Patologia)Multidisciplinarymedicine.diagnostic_testQFatty AcidsChromatographic TechniquesRDegeneration (Pathology)Animal ModelsLipidsChemistrymedicine.anatomical_structureNeurologyDocosahexaenoic acidPhysical SciencesMedicineRetinal DisordersRabbitsSafetyAnatomyResearch Articlemedicine.medical_specialtyHistologyDrug Research and DevelopmentDocosahexaenoic AcidsNew Zealand AlbinoScienceOcular AnatomyResearch and Analysis MethodsRetinaInjectionsAqueous HumorModel OrganismsOcular SystemElectroretinographyToxicity Tests AcutemedicineAnimalsFatty acidsGas ChromatographyPharmacologyDose-Response Relationship Drugbusiness.industrySignificant differenceBiology and Life SciencesRetinalmedicine.diseaseSurgeryVitreous BodyOphthalmologychemistryNeuro-OphthalmologyAnimal experimentationRabbit modelClinical MedicinebusinessElectroretinographyPLoS ONE
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Involvement of plasmalogens in post-natal retinal vascular development

2014

Objective: Proper development of retinal blood vessels is essential to ensure sufficient oxygen and nutrient supplies to the retina. It was shown that polyunsaturated fatty acids (PUFAs) could modulate factors involved in tissue vascularization. A congenital deficiency in ether-phospholipids, also termed "plasmalogens'', was shown to lead to abnormal ocular vascularization. Because plasmalogens are considered to be reservoirs of PUFAs, we wished to improve our understanding of the mechanisms by which plasmalogens regulate retinal vascular development and whether the release of PUFAs by calcium-independent phospholipase A2 (iPLA2) could be involved. [br/] Methods and Results: By characterizi…

MaleretinaOrganes des sensAngiogenesis[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionlcsh:MedicineRetinal NeovascularizationBiochemistryImmunoenzyme TechniquesMicechemistry.chemical_compoundangiogenesisMedicine and Health Sciencesangiogenesis;astrocytes;capillaries;endothelial cells;gene expression;phospholipids;retina;retinal vesselscapillarieslcsh:ScienceCells CulturedOligonucleotide Array Sequence AnalysisMice KnockoutMultidisciplinarymedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionLipidsendothelial cellsCell biologyEndothelial stem cellmedicine.anatomical_structureBiochemistry[ SDV.MHEP.OS ] Life Sciences [q-bio]/Human health and pathology/Sensory OrgansAlimentation et NutritionFatty Acids UnsaturatedRetinal DisordersFemaleResearch ArticleAstrocyteEndotheliumSensory OrgansPlasmalogensBiologyReal-Time Polymerase Chain ReactionGroup VI Phospholipases A2AngiopoietinElectroretinographymedicineFood and NutritionAnimalsRNA Messenger[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory OrgansphospholipidsRetinaGene Expression Profilinglcsh:Rretinal vesselsastrocytesBiology and Life SciencesRetinalMice Inbred C57BLOphthalmologyAnimals Newbornchemistrygene expressionlcsh:QEndothelium Vascular[SDV.AEN]Life Sciences [q-bio]/Food and NutritionAcyltransferasesBiomarkersDevelopmental BiologyElectroretinography
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Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells.

2012

PURPOSE: Previous studies show significantly specifically changed autoantibody reactions against retinal antigens in the serum of glaucoma and ocular hypertension (OHT) patients in comparison to healthy people. As pathogenesis of glaucoma still is unknown the aim of this study was to analyze if the serum and antibodies of glaucoma patients interact with neuroretinal cells. METHODS: R28 cells were incubated with serum of patients suffering from primary open angle glaucoma (POAG), normal tension glaucoma (NTG) or OHT, POAG serum after antibody removal and serum from healthy people for 48 h under a normal or an elevated pressure of 15000 Pa (112 mmHg). RGC5 cells were additionally incubated wi…

ProteomicsRetinal Ganglion CellsSerumProteomegenetic structuresOcular hypertensionGlaucomalcsh:MedicineAutoimmunityPathogenesischemistry.chemical_compoundMolecular Cell Biologylcsh:ScienceCellular Stress ResponsesMultidisciplinarySpectrometric Identification of ProteinsbiologyNeurodegenerative DiseasesBlood proteinsSignaling CascadesNeurologyMedicineRetinal DisordersElectrophoresis Polyacrylamide GelAntibodyGlaucoma Open-AngleRetinal NeuronsSignal TransductionResearch ArticleSpectrometry Mass Electrospray IonizationImmunologyImmunoglobulinsPeptide MappingAntibodiesStress Signaling CascadeCell LineAntigenmedicinePressureAnimalsHumansBiologylcsh:RAutoantibodyRetinalGlaucomamedicine.diseaseeye diseasesRatsOphthalmologychemistrySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationImmunologybiology.proteinOcular HypertensionClinical Immunologylcsh:Qsense organsChromatography LiquidPLoS ONE
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Genetic variants linked to myopic macular degeneration in persons with high myopia: CREAM Consortium.

2019

Purpose: To evaluate the roles of known myopia-associated genetic variants for development of myopic macular degeneration (MMD) in individuals with high myopia (HM), using case-control studies from the Consortium of Refractive Error and Myopia (CREAM). Methods: A candidate gene approach tested 50 myopia-associated loci for association with HM and MMD, using meta-analyses of case-control studies comprising subjects of European and Asian ancestry aged 30 to 80 years from 10 studies. Fifty loci with the strongest associations with myopia were chosen from a previous published GWAS study. Highly myopic (spherical equivalent [SE] ≤ -5.0 diopters [D]) cases with MMD (N = 348), and two sets of cont…

Refractive errorCandidate genegenetic structuresEmmetropiaGenome-wide association studySensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Macular DegenerationMathematical and Statistical TechniquesMedicine and Health SciencesMyopiaGeriatric OphthalmologyDioptreVisual ImpairmentsAged 80 and overMultidisciplinaryQRetinal DegenerationStatisticsRGenomicsMetaanalysisPhenotypeResearch DesignPhysical SciencesMedicineRetinal DisordersFemaleAnatomyResearch Articlemedicine.medical_specialtyScienceOcular AnatomySingle-nucleotide polymorphismResearch and Analysis MethodsRetinaOcular SystemOphthalmologyGeneticsGenome-Wide Association StudiesmedicineHumansStatistical Methodsbusiness.industryGene Expression ProfilingCase-control studyBiology and Life SciencesComputational BiologyGenetic VariationCorrectionHuman GeneticsMacular degenerationGenome Analysismedicine.diseaseeye diseasesOphthalmologyGenetic LociGeriatricsMacular DisordersCase-Control StudiesEyessense organsbusinessHeadMathematicsPloS one
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Neurosteroids in the Retina

2003

Steroids may have a powerful role in neuronal degeneration. Recent research has revealed that steroids may influence the onset and progression of some retinal disorders as well as neurodegenerative diseases and, as in brain, they accumulate in the retina via a local synthesis (neurosteroids) and metabolism of blood-circulating steroid hormones. Their crucial role as neurodegenerative and neuroprotective agents has been also upheld in a retinal excitotoxic paradigm. These findings are reviewed especially from the emerging perspective that after an insult local changes in steroidogenic responses and consequent neurosteroid availability might turn out to be offensive or defensive cellular adap…

RetinaRetinal DisorderNeuroactive steroidGeneral NeuroscienceLong-term potentiationRetinalBiologyNeuroprotectionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundmedicine.anatomical_structureHistory and Philosophy of SciencechemistrymedicinePregnenolone sulfateNeuroscienceHormoneAnnals of the New York Academy of Sciences
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Translational read-through as an alternative approach for ocular gene therapy of retinal dystrophies caused by in-frame nonsense mutations

2014

AbstractThe eye has become an excellent target for gene therapy, and gene augmentation therapy of inherited retinal disorders has made major progress in recent years. Nevertheless, a recent study indicated that gene augmentation intervention might not stop the progression of retinal degeneration in patients. In addition, for many genes, viral-mediated gene augmentation is currently not feasible due to gene size and limited packaging capacity of viral vectors as well as expression of various heterogeneous isoforms of the target gene. Thus, alternative gene-based strategies to stop or delay the retinal degeneration are necessary. This review focuses on an alternative pharmacologic treatment s…

Retinal degenerationGeneticsGene isoformOxadiazolesRetinal DisorderPhysiologyNonsense mutationContext (language use)Genetic TherapyBiologyBioinformaticsmedicine.diseaseSensory SystemsAminoglycosidesCodon NonsenseProtein BiosynthesisRetinal DystrophiesmedicineAnimalsHumansCoding regionGeneRetinal DystrophiesSignal TransductionVisual Neuroscience
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