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 ResearchMeSH KeywordsAnimalsFatty AcidsFibrosisKidney DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsOxidation-ReductionConceptsFatty 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 oxidation
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
Mutation of POLB Causes Lupus in Mice
Senejani AG, Liu Y, Kidane D, Maher SE, Zeiss CJ, Park HJ, Kashgarian M, McNiff JM, Zelterman D, Bothwell AL, Sweasy JB. Mutation of POLB Causes Lupus in Mice. Cell Reports 2014, 6: 1-8. PMID: 24388753, PMCID: PMC3916967, DOI: 10.1016/j.celrep.2013.12.017.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusLupus-like diseaseLupus erythematosusAutoimmune pathologyMouse modelGenome-wide association studiesPol β activityDecreased expressionMutant miceUnderlying causeMicePrevious genome-wide association studyΒ activityDNA polymerase activityReplication studyExcision repair pathwayImmune diversitySomatic hypermutationBase excision repair pathwayAssociation studiesErythematosusLupusPolymerase activityExpressionKey enzyme
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
Maropitant 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
2010
REVIEW PAPER: Animals as Models of Age-Related Macular Degeneration
Zeiss CJ. REVIEW PAPER: Animals as Models of Age-Related Macular Degeneration. Veterinary Pathology 2010, 47: 396-413. PMID: 20382825, DOI: 10.1177/0300985809359598.Peer-Reviewed Original ResearchConceptsAge-related macular degenerationMacular degenerationRelevant mouse modelNonhuman primate modelCause of blindnessRetinal pigment epitheliumMajority of casesEtiologic complexityAMD pathologyChoroidal neovascularizationEtiologic factorsModel of agePrimate modelRodent retinaPathogenetic mechanismsMouse modelGenetic predispositionSalient anatomyPigment epitheliumAnimal modelsDegenerative conditionsComplement activationLipid metabolismBruch's membraneGene function
2009
Embryonic arrest at midgestation and disruption of Notch signaling produced by the absence of both epsin 1 and epsin 2 in mice
Chen H, Ko G, Zatti A, Di Giacomo G, Liu L, Raiteri E, Perucco E, Collesi C, Min W, Zeiss C, De Camilli P, Cremona O. Embryonic arrest at midgestation and disruption of Notch signaling produced by the absence of both epsin 1 and epsin 2 in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 13838-13843. PMID: 19666558, PMCID: PMC2728981, DOI: 10.1073/pnas.0907008106.Peer-Reviewed Original ResearchConceptsEndocytic adaptorsRole of epsinsClathrin-mediated endocytosisSpecific membrane proteinsDouble knockout embryosPrimary target genesBeginning of organogenesisActivation of NotchEmbryonic lethalityPutative functionsKnockout embryosEmbryonic arrestMembrane proteinsGenetic approachesTarget genesDKO embryosNotch activationNotch signalingEndocytic functionDevelopmental defectsGenesEpsinEmbryosInactivation resultsEndocytosis
2004
Caspase-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 labelingProliferation of Microglia, but not Photoreceptors, in the Outer Nuclear Layer of the rd-1 Mouse
Zeiss CJ, Johnson EA. Proliferation of Microglia, but not Photoreceptors, in the Outer Nuclear Layer of the rd-1 Mouse. Investigative Ophthalmology & Visual Science 2004, 45: 971-976. PMID: 14985319, DOI: 10.1167/iovs.03-0301.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBiomarkersCDC2-CDC28 KinasesCell Cycle ProteinsCell DivisionCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent KinasesDNA ReplicationImmunohistochemistryIn Situ Nick-End LabelingKi-67 AntigenMiceMice, Inbred C57BLMice, Mutant StrainsMicrogliaPhotoreceptor Cells, VertebrateProliferating Cell Nuclear AntigenProto-Oncogene ProteinsRetinal DegenerationConceptsOuter nuclear layerTerminal dUTP transferase nick end labelingNuclear layerCell cycle progressionMicroglial cellsPhotoreceptor deathCycle progressionProliferation of microgliaNick end labelingCell nuclear antigenControl miceNeurotrophic factorPeripheral gradientInner retinaNeuronal deathCell cycle proteinsPhotoreceptor lossRD-1Ki-67Postnatal dayPreexisting conditionsNeurodegenerative conditionsDouble immunolabelingBromodeoxyuridine uptakePhotoreceptor apoptosis