2021
Modeling SARS-CoV-2 propagation using rat coronavirus-associated shedding and transmission
Zeiss CJ, Asher JL, Vander Wyk B, Allore HG, Compton SR. Modeling SARS-CoV-2 propagation using rat coronavirus-associated shedding and transmission. PLOS ONE 2021, 16: e0260038. PMID: 34813610, PMCID: PMC8610237, DOI: 10.1371/journal.pone.0260038.Peer-Reviewed Original ResearchConceptsViral sheddingSialodacryoadenitis virusSARS-CoV-2Prior natural infectionSARS-CoV-2 propagationSeropositive animalsLow-level sheddingNaive recipient ratsCOVID-19Cycle threshold valuesDirect contact exposureSeroconversion ratesReinfected animalsRecipient ratsImmune protectionHigh riskNaive animalsSusceptible individualsInitial infectionGlobal immunityExposure paradigmRat coronavirusNatural infectionInfectionRatsAge‐related calcium dysregulation linked with tau pathology and impaired cognition in non‐human primates
Datta D, Leslie SN, Wang M, Morozov YM, Yang S, Mentone S, Zeiss C, Duque A, Rakic P, Horvath TL, van Dyck C, Nairn AC, Arnsten AFT. Age‐related calcium dysregulation linked with tau pathology and impaired cognition in non‐human primates. Alzheimer's & Dementia 2021, 17: 920-932. PMID: 33829643, PMCID: PMC8195842, DOI: 10.1002/alz.12325.Peer-Reviewed Original ResearchConceptsTau pathologyCalcium leakTau phosphorylationNeuronal firingAlzheimer's diseaseEarly tau phosphorylationPyramidal cell dendritesSporadic Alzheimer's diseasePrimary cortical neuronsPotential therapeutic targetCognitive performanceAge-related reductionMacaque dorsolateral prefrontal cortexDorsolateral prefrontal cortexNon-human primatesCalcium dysregulationCell dendritesCortical neuronsCalcium-binding proteinsAD biomarkersPathology markersTherapeutic targetAnimal modelsAged monkeysPrefrontal cortex
2020
AgRP neurons control compulsive exercise and survival in an activity-based anorexia model
Miletta MC, Iyilikci O, Shanabrough M, Šestan-Peša M, Cammisa A, Zeiss CJ, Dietrich MO, Horvath TL. AgRP neurons control compulsive exercise and survival in an activity-based anorexia model. Nature Metabolism 2020, 2: 1204-1211. PMID: 33106687, DOI: 10.1038/s42255-020-00300-8.Peer-Reviewed Original ResearchConceptsAgRP neuronsActivity-based anorexia modelAgRP neuronal activityVivo fiber photometryFood-restricted miceFood-restricted animalsCompulsive exerciseAnorexia modelHypothalamic agoutiNeuropeptide YExercise volumeFood intakeMouse modelNeuronal activityFiber photometryDaily activationNeuronal circuitsPsychiatric conditionsAnorexia nervosaChemogenetic toolsNeuronsLong-term behavioral impactElevated fat contentVoluntary cessationFat content
2019
Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis
Price NL, Miguel V, Ding W, Singh AK, Malik S, Rotllan N, Moshnikova A, Toczek J, Zeiss C, Sadeghi MM, Arias N, Baldán Á, Andreev OA, Rodríguez-Puyol D, Bahal R, Reshetnyak YK, Suárez Y, Fernández-Hernando C, Lamas S. Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis. JCI Insight 2019, 4 PMID: 31613798, PMCID: PMC6948871, DOI: 10.1172/jci.insight.131102.Peer-Reviewed Original ResearchConceptsFatty acid oxidationChronic kidney diseaseKidney diseaseDisease progressionMiR-33Bone marrow transplantExtent of fibrosisDevelopment of fibrosisAttractive therapeutic targetExpression of factorsNucleic acid inhibitorsMarrow transplantKidney fibrosisFibrotic kidneysMouse modelTherapeutic targetLipid metabolismPharmacological inhibitionFibrosisLipid accumulationDiseaseGenetic deficiencyProgressionKidneyAcid oxidationDoxorubicin-Induced Cardiotoxicity in Collaborative Cross (CC) Mice Recapitulates Individual Cardiotoxicity in Humans
Zeiss CJ, Gatti DM, Toro-Salazar O, Davis C, Lutz CM, Spinale F, Stearns T, Furtado MB, Churchill GA. Doxorubicin-Induced Cardiotoxicity in Collaborative Cross (CC) Mice Recapitulates Individual Cardiotoxicity in Humans. G3: Genes, Genomes, Genetics 2019, 9: 2637-2646. PMID: 31263061, PMCID: PMC6686936, DOI: 10.1534/g3.119.400232.Peer-Reviewed Original ResearchConceptsCardiac diseaseCardiac pathologyCardiac troponin I levelsUltimate severityChronic cardiac injuryTroponin I levelsPotential predictive biomarkersDoxorubicin-Induced CardiotoxicityComplete blood countPanel of biomarkersCurrent mouse modelsEffect of treatmentCardiac troponin IProgressive cardiotoxicityLight chain 3Acute periodAcute phaseCardiac injuryRenal toxicityBlood countPredictive biomarkersChronic timepointsCollaborative Cross miceSame doseI levelsAn ABCA4 loss-of-function mutation causes a canine form of Stargardt disease
Mäkeläinen S, Gòdia M, Hellsand M, Viluma A, Hahn D, Makdoumi K, Zeiss CJ, Mellersh C, Ricketts SL, Narfström K, Hallböök F, Ekesten B, Andersson G, Bergström TF. An ABCA4 loss-of-function mutation causes a canine form of Stargardt disease. PLOS Genetics 2019, 15: e1007873. PMID: 30889179, PMCID: PMC6424408, DOI: 10.1371/journal.pgen.1007873.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsATP Binding Cassette Transporter, Subfamily A, Member 4ATP-Binding Cassette TransportersBase SequenceCodon, NonsenseDisease Models, AnimalDog DiseasesDogsFemaleGenes, RecessiveHomozygoteHumansLipofuscinMacular DegenerationMaleMicroscopy, FluorescenceModels, MolecularMutagenesis, InsertionalMutationPedigreeProtein ConformationRetinaStargardt DiseaseWhole Genome SequencingConceptsRetinal pigment epitheliumStargardt diseaseAutosomal recessive retinal degenerative diseaseRetinal degenerationABCA4 geneVisual impairmentCentral visual impairmentFull-length ABCA4 proteinFunction mutationsLabrador Retriever dogsLarge animal modelRetinal degenerative diseasesAutosomal recessive retinal degenerationMember 4 geneRecessive retinal degenerationStandard treatmentClinical trialsClinical signsLipofuscin depositsPigment epitheliumAnimal modelsCanine modelUnaffected dogsAffected dogsCone photoreceptors
2017
Established patterns of animal study design undermine translation of disease-modifying therapies for Parkinson’s disease
Zeiss CJ, Allore HG, Beck AP. Established patterns of animal study design undermine translation of disease-modifying therapies for Parkinson’s disease. PLOS ONE 2017, 12: e0171790. PMID: 28182759, PMCID: PMC5300282, DOI: 10.1371/journal.pone.0171790.Peer-Reviewed Original ResearchConceptsDisease-modifying therapiesClinical outcome measuresDisease-modifying interventionsNon-human primatesParkinson's diseaseOutcome measuresStudy designHuman studiesToxin-induced modelsHuman interventional studiesLongitudinal clinical outcomesPreclinical study designStudy design dataToxic protocolsClinical outcomesContemporary cohortNeuropathologic dataStudy design factorsInterventional studyMultiple time pointsPD phenotypeAnimal studiesIntervention characteristicsIntervention categoriesProgressive nature
2015
Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway
Sati L, Zeiss C, Yekkala K, Demir R, McGrath J. Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway. Molecular And Cellular Biology 2015, 35: 3436-3445. PMID: 26169830, PMCID: PMC4561735, DOI: 10.1128/mcb.00381-15.Peer-Reviewed Original ResearchConceptsGrowth factor β pathwayHuman vascular malformationsTestis-expressed genesΒ pathwayParalog of CTCFEmbryonic stem cellsTransforming Growth Factor-β PathwayPrior mouse modelsMouse embryogenesisBioinformatics analysisCancer-testis antigensDownstream targetsES cellsPostnatal lethalityCTCFLEmbryogenesis resultsTGFB pathwayGenesStem cellsVascular defectsPathwayExpressionTransgenic miceEye malformationsPhenotype
2014
Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice
Kim JD, Toda C, D’Agostino G, Zeiss CJ, DiLeone RJ, Elsworth JD, Kibbey RG, Chan O, Harvey BK, Richie CT, Savolainen M, Myöhänen T, Jeong JK, Diano S. Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 11876-11881. PMID: 25071172, PMCID: PMC4136568, DOI: 10.1073/pnas.1406000111.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood GlucoseGene ExpressionGene Knockdown TechniquesGlucagonGlucose Clamp TechniqueGlucose IntoleranceHypothalamusIndolesInsulinInsulin SecretionIon ChannelsMaleMiceMice, TransgenicMitochondrial ProteinsPancreasPhosphorylationProlyl OligopeptidasesReceptor, InsulinRecombinant ProteinsSerine EndopeptidasesSerine Proteinase InhibitorsThiazolidinesUncoupling Protein 1Ventromedial Hypothalamic NucleusConceptsWild-type miceGlucose intoleranceGlucagon secretionProlyl endopeptidaseHyperinsulinemic-euglycemic clamp studiesWild-type control miceGlucose-induced insulin releaseGlucose-induced insulin secretionEuglycemic clamp studiesAutonomic nervous systemVMH injectionsSympathetic outflowWild-type controlsNorepinephrine levelsGlucagon levelsGlucose toleranceControl miceInsulin levelsCentral infusionPancreatic functionVentromedial nucleusInsulin secretionNeuronal activationGlucose-intolerant phenotypeCentral regulation
2013
MyD88 Deficiency Markedly Worsens Tissue Inflammation and Bacterial Clearance in Mice Infected with Treponema pallidum, the Agent of Syphilis
Silver AC, Dunne DW, Zeiss CJ, Bockenstedt LK, Radolf JD, Salazar JC, Fikrig E. MyD88 Deficiency Markedly Worsens Tissue Inflammation and Bacterial Clearance in Mice Infected with Treponema pallidum, the Agent of Syphilis. PLOS ONE 2013, 8: e71388. PMID: 23940747, PMCID: PMC3734110, DOI: 10.1371/journal.pone.0071388.Peer-Reviewed Original ResearchConceptsMyD88-deficient miceTreponema pallidumMyD88-deficient animalsResistance of miceToll-like receptorsWild-type miceMyD88-deficient macrophagesMacrophage-mediated clearanceHigh pathogen burdenMyD88 deficiencySpirochete Treponema pallidumWT miceTissue infiltratesBacterial clearanceExtensive inflammationTissue inflammationPlasma cellsControl animalsWT macrophagesMost TLRsAnimal modelsMixed mononuclearPathogen burdenMiceT. pallidum
2011
A slowly progressive retinopathy in the Shetland Sheepdog
Karlstam L, Hertil E, Zeiss C, Ropstad EO, Bjerkås E, Dubielzig RR, Ekesten B. A slowly progressive retinopathy in the Shetland Sheepdog. Veterinary Ophthalmology 2011, 14: 227-238. PMID: 21733063, DOI: 10.1111/j.1463-5224.2010.00866.x.Peer-Reviewed Original ResearchConceptsB-wave amplitudeRod-cone degenerationOphthalmoscopic signsProgressive retinopathyProgressive retinal atrophyShetland SheepdogsTapetal fundusOphthalmoscopic changesRetinal atrophyProgressive rod-cone degenerationSlit-lamp biomicroscopyOuter nuclear layerOphthalmoscopic findingsOphthalmic examinationNuclear layerNormal dogsCone outer segmentsGreyish discolorationRepeated examinationsAbnormal appearanceVisual impairmentRetinopathyDogsMicroscopic examinationForty adultsMaropitant citrate for treatment of ulcerative dermatitis in mice with a C57BL/6 background.
Williams-Fritze MJ, Carlson Scholz JA, Zeiss C, Deng Y, Wilson SR, Franklin R, Smith PC. Maropitant citrate for treatment of ulcerative dermatitis in mice with a C57BL/6 background. Journal Of The American Association For Laboratory Animal Science 2011, 50: 221-6. PMID: 21439216, PMCID: PMC3061423.Peer-Reviewed Original ResearchConceptsMaropitant citrateSubstance PUlcerative dermatitisC57BL/6 backgroundInhibition of SPCommon progressive conditionItch-scratch cycleNK1 receptor antagonistNeurokinin-1 receptorTachykinin neurokinin-1 receptorUD lesionsItch sensationExact etiologyInflamed skinReceptor antagonistNK1 receptorsProgressive conditionDorsal neckSkin traumaAdditional traumaTherapeutic interventionsImportant neuropeptideMiceDermatitisLesions
2009
CREB1/ATF1 Activation in Photoreceptor Degeneration and Protection
Beltran WA, Allore HG, Johnson E, Towle V, Tao W, Acland GM, Aguirre GD, Zeiss CJ. CREB1/ATF1 Activation in Photoreceptor Degeneration and Protection. Investigative Ophthalmology & Visual Science 2009, 50: 5355-5363. PMID: 19643965, PMCID: PMC3172238, DOI: 10.1167/iovs.09-3741.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 1AgedAged, 80 and overAnimalsArrestinCell CountCiliary Neurotrophic FactorCyclic AMP Response Element-Binding ProteinDog DiseasesDogsFemaleGenotypeHumansImmunoblottingImmunoenzyme TechniquesMacular DegenerationMalePhosphorylationPhotoreceptor Cells, VertebrateRetinitis PigmentosaRhodopsinConceptsAge-related macular degenerationCiliary neurotrophic factorNormal canine retinaRcd1 dogsCanine retinaHuman retinaInnate protective responseNeuroprotective stimulusInner retinaNeurotrophic factorTranscription factor 1Macular degenerationRetinal protectionPhotoreceptor protectionP-CREB1Photoreceptor diseaseNormal dogsCanine modelPhotoreceptor degenerationRetinal degenerationProtective responseStrong immunolabelingCone photoreceptorsPhotoreceptor nucleiRetina
2007
Motor deficits and altered striatal gene expression in aphakia (ak) mice
Singh B, Wilson JH, Vasavada HH, Guo Z, Allore HG, Zeiss CJ. Motor deficits and altered striatal gene expression in aphakia (ak) mice. Brain Research 2007, 1185: 283-292. PMID: 17949697, PMCID: PMC3904435, DOI: 10.1016/j.brainres.2007.09.006.Peer-Reviewed Original ResearchConceptsSubstantia nigra pars compactaMonths of lifeAK miceWT miceParkinson's diseaseMotor performanceStriatal gene expressionDopaminergic denervationNigrostriatal dysfunctionStriatal denervationMotor deficitsPars compactaMotor abnormalitiesAphakia miceMice progressMotor functionStriatal transcriptomeDRD2 expressionPole testWT controlsSemi-quantitative RT-PCRAge groupsMiceRT-PCRTime points
2006
Safety of Recombinant Adeno-Associated Virus Type 2–RPE65 Vector Delivered by Ocular Subretinal Injection
Jacobson SG, Acland GM, Aguirre GD, Aleman TS, Schwartz SB, Cideciyan AV, Zeiss CJ, Komaromy AM, Kaushal S, Roman AJ, Windsor EA, Sumaroka A, Pearce-Kelling SE, Conlon TJ, Chiodo VA, Boye SL, Flotte TR, Maguire AM, Bennett J, Hauswirth WW. Safety of Recombinant Adeno-Associated Virus Type 2–RPE65 Vector Delivered by Ocular Subretinal Injection. Molecular Therapy 2006, 13: 1074-1084. PMID: 16644289, DOI: 10.1016/j.ymthe.2006.03.005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedBlindnessCarrier ProteinsCis-trans-IsomerasesDependovirusDogsDose-Response Relationship, DrugDrug-Related Side Effects and Adverse ReactionsEye ProteinsFemaleGenetic TherapyGenetic VectorsInjections, IntralesionalMaleOptic Atrophy, Hereditary, LeberRatsRats, Sprague-DawleyRecombinant ProteinsRetinaTissue DistributionConceptsRPE65-mutant dogsLeber congenital amaurosisMonths postinjectionHuman trialsBiodistribution studiesVector dosesHigh vector dosesOcular examinationRetinal histopathologyInjected eyeOptic nerveDose-response resultsModerate inflammationNormal ratsTraumatic lesionsDose efficacyVisual centersSubretinal injectionRPE65 geneSystemic toxicityVirus typeCongenital amaurosisOcular deliveryPostinjectionDoses
2005
Complement Factor H Polymorphism in Age-Related Macular Degeneration
Klein RJ, Zeiss C, Chew EY, Tsai JY, Sackler RS, Haynes C, Henning AK, SanGiovanni JP, Mane SM, Mayne ST, Bracken MB, Ferris FL, Ott J, Barnstable C, Hoh J. Complement Factor H Polymorphism in Age-Related Macular Degeneration. Science 2005, 308: 385-389. PMID: 15761122, PMCID: PMC1512523, DOI: 10.1126/science.1109557.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overAgingAllelesAmino Acid SubstitutionCase-Control StudiesChoroidChromosomes, Human, Pair 1Complement Factor HComplement Membrane Attack ComplexExonsFemaleGenetic MarkersGenetic Predisposition to DiseaseGenotypeHaplotypesHistidineHumansImmunity, InnateIntronsLinkage DisequilibriumMacular DegenerationMaleOligonucleotide Array Sequence AnalysisPigment Epithelium of EyePolymorphism, GeneticPolymorphism, Single NucleotideRisk FactorsSmokingConceptsAge-related macular degenerationComplement factor H (CFH) geneMacular degenerationLikelihood of AMDComplement Factor H PolymorphismRisk allelesC-reactive proteinFactor H geneAmino acids 402H polymorphismCFH geneFamily-based studyMajor causeSingle nucleotide polymorphismsCommon variantsDegenerationPolymorphismH gene
2004
A morphologic study of intravitreal membranes associated with intraocular hemorrhage in the dog
Zeiss CJ, Dubielzig RR. A morphologic study of intravitreal membranes associated with intraocular hemorrhage in the dog. Veterinary Ophthalmology 2004, 7: 239-243. PMID: 15200620, DOI: 10.1111/j.1463-5224.2004.04033.x.Peer-Reviewed Original ResearchConceptsGlial fibrillary acidic proteinSmooth muscle actinRetinal neovascularizationIntravitreal hemorrhageMuscle actinFactor VIII-related antigenIntravitreal membranesAdditional common findingsOptic disc cuppingVIII-related antigenFibrillary acidic proteinDisc cuppingIntraocular hemorrhageFibrovascular membranesCommon findingEpiretinal membraneGlial originHemorrhageImmunohistochemical proceduresSpringer spanielAcidic proteinLabrador RetrieversStandard histologyMorphologic studiesDogsCaspase-3 in Postnatal Retinal Development and Degeneration
Zeiss CJ, Neal J, Johnson EA. Caspase-3 in Postnatal Retinal Development and Degeneration. Investigative Ophthalmology & Visual Science 2004, 45: 964-970. PMID: 14985318, DOI: 10.1167/iovs.03-0439.Peer-Reviewed Original ResearchConceptsTerminal dUTP transferase nick end labelingPostnatal retinal developmentCaspase-3Photoreceptor degenerationRod deathMutant miceRetinal developmentInner nuclear layerDouble mutant miceNick end labelingLight microscopic levelRod photoreceptor developmentCell nuclear antigenNeonatal deathRetinal morphometryDysplastic lesionsRetinal dysplasiaNuclear layerPhotoreceptor protectionImmunohistochemical stainingRodent modelsFactor VIICaspase-3 activationNuclear antigenEnd labeling
2003
Feline Intraocular Tumors May Arise from Transformation of Lens Epithelium
Zeiss CJ, Johnson EM, Dubielzig RR. Feline Intraocular Tumors May Arise from Transformation of Lens Epithelium. Veterinary Pathology 2003, 40: 355-362. PMID: 12824506, DOI: 10.1354/vp.40-4-355.Peer-Reviewed Original ResearchConceptsSmooth muscle actinIntraocular sarcomaCollagen type IVMuscle actinGlial fibrillary acidic proteinMalignant intraocular neoplasmNerve growth factor receptorBasement membrane-type materialType IVFibrillary acidic proteinYears of ageExpression of vimentinEpithelial-mesenchymal phenotypeCell of originNeural cell adhesion moleculeExpression of desminGrowth factor receptorOcular traumaImmunohistochemical phenotypeIntraocular neoplasmPathophysiologic similaritiesUndifferentiated sarcomaEpithelial neoplasiaIntraocular tumorsMelan A