2021
DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model
Paluri SL, Burak M, Senejani AG, Levinson M, Rahim T, Clairmont K, Kashgarian M, Alvarado-Cruz I, Meas R, Cardó-Vila M, Zeiss C, Maher S, Bothwell ALM, Coskun E, Kant M, Jaruga P, Dizdaroglu M, Lloyd R, Sweasy JB. DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model. DNA Repair 2021, 105: 103152. PMID: 34186496, PMCID: PMC8635285, DOI: 10.1016/j.dnarep.2021.103152.Peer-Reviewed Original ResearchAnimal Models of COVID-19 II. Comparative Immunology
Veenhuis RT, Zeiss CJ. Animal Models of COVID-19 II. Comparative Immunology. ILAR Journal 2021, 62: ilab010-. PMID: 33914873, PMCID: PMC8135340, DOI: 10.1093/ilar/ilab010.Peer-Reviewed Original ResearchConceptsSARS-CoV-2Animal modelsLarge animal modelCytokine surgeCell infiltrationAcute respiratory syndrome coronavirus 2 infectionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectionSyndrome coronavirus 2 infectionSevere coronavirus disease 2019SARS-CoV-2 infectionCoronavirus 2 infectionT cell responsesImmune cell infiltrationStrong antibody responseAnimal model studiesCoronavirus disease 2019Large animal model studyImmunological questionsHigh mortality rateCOVID-19Small animal modelsImmune system functionAfrican green monkeysSARS-CoV-2 researchVaccine efficacyAnimal Models of COVID-19. I. Comparative Virology and Disease Pathogenesis
Zeiss CJ, Compton S, Veenhuis RT. Animal Models of COVID-19. I. Comparative Virology and Disease Pathogenesis. ILAR Journal 2021, 62: ilab007-. PMID: 33836527, PMCID: PMC8083356, DOI: 10.1093/ilar/ilab007.Peer-Reviewed Original ResearchConceptsSARS-CoV-2SARS-CoVViral sheddingImmune responseSpontaneous modelAnimal modelsDisease pathogenesisSARS-CoV-2 infectionCOVID-19Severe acute respiratory syndrome coronavirusAcute respiratory syndrome coronavirusChimeric SARS-CoVRole of comorbiditiesCoronavirus disease 2019 (COVID-19) pandemicShort-term immune responseWild-type miceSeverity of diseaseOrgan-specific pathologySARS-CoV-2 virusDisease 2019 pandemicAfrican green monkeysTest therapeuticsVaccine approachesNonfatal diseaseTissue involvement
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 levels
2017
Bridging the Gap between Reproducibility and Translation: Data Resources and Approaches.
Zeiss CJ, Johnson LK. Bridging the Gap between Reproducibility and Translation: Data Resources and Approaches. ILAR Journal 2017, 58: 1-3. PMID: 28586416, DOI: 10.1093/ilar/ilx017.Peer-Reviewed Original ResearchEstablished 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
Loss of endogenous Nfatc1 reduces the rate of DMBA/TPA-induced skin tumorigenesis
Goldstein J, Roth E, Roberts N, Zwick R, Lin S, Fletcher S, Tadeu A, Wu C, Beck A, Zeiss C, Suárez-Fariñas M, Horsley V. Loss of endogenous Nfatc1 reduces the rate of DMBA/TPA-induced skin tumorigenesis. Molecular Biology Of The Cell 2015, 26: 3606-3614. PMID: 26310443, PMCID: PMC4603931, DOI: 10.1091/mbc.e15-05-0282.Peer-Reviewed Original ResearchConceptsDMBA/TPA-induced skin tumorigenesisFollicular stem cellsSkin tumorigenesisDMBA metabolismDMBA-induced DNA damageSquamous cell carcinoma formationSkin squamous cell carcinomaStem cellsSquamous cell carcinomaEndogenous expressionRate of tumorigenesisImmunosuppressive therapyCalcineurin inhibitorsCell carcinomaSkin tumorsHigh incidenceCarcinoma formationHair follicle bulge stem cellsMiceNFATc1Tumor initiationActive NFATc1Suppress tumorigenesisBulge stem cellsInducible deletionClostridium perfringens enterotoxin C‐terminal domain labeled to fluorescent dyes for in vivo visualization of micrometastatic chemotherapy‐resistant ovarian cancer
Cocco E, Shapiro EM, Gasparrini S, Lopez S, Schwab CL, Bellone S, Bortolomai I, Sumi NJ, Bonazzoli E, Nicoletti R, Deng Y, Saltzman WM, Zeiss CJ, Centritto F, Black JD, Silasi DA, Ratner E, Azodi M, Rutherford TJ, Schwartz PE, Pecorelli S, Santin AD. Clostridium perfringens enterotoxin C‐terminal domain labeled to fluorescent dyes for in vivo visualization of micrometastatic chemotherapy‐resistant ovarian cancer. International Journal Of Cancer 2015, 137: 2618-2629. PMID: 26060989, PMCID: PMC4573336, DOI: 10.1002/ijc.29632.Peer-Reviewed Original ResearchConceptsPatient-derived xenograftsTumor fluorescenceChemotherapy-resistant ovarian cancerClaudin-3Human ovarian cancer xenograftsTime of surgeryOvarian cancer patientsNeoadjuvant chemotherapy treatmentOvarian cancer xenograftsHealthy organsVivo visualizationTime of intervalBackground fluorescence ratioClostridium perfringens enterotoxinChemotherapy-naïveMicrometastatic diseaseMalignant ascitesOvarian diseaseResidual diseaseOvarian tumorsCancer patientsCancer xenograftsChemotherapy treatmentIP injectionOvarian cancer
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 regulationMutation 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
Poliomyelitis in MuLV-infected ICR-SCID mice after injection of basement membrane matrix contaminated with lactate dehydrogenase-elevating virus.
Carlson Scholz JA, Garg R, Compton SR, Allore HG, Zeiss CJ, Uchio EM. Poliomyelitis in MuLV-infected ICR-SCID mice after injection of basement membrane matrix contaminated with lactate dehydrogenase-elevating virus. Comparative Medicine 2011, 61: 404-11. PMID: 22330347, PMCID: PMC3193062.Peer-Reviewed Original ResearchConceptsAge-dependent poliomyelitisClinical signsDehydrogenase-elevating virusICR-SCID miceSpinal cordRT-PCRMurine leukemia virusLife-long viremiaLactate dehydrogenase-elevating virusLeukemia virusVentral spinal cordEndogenous murine leukemia virusPCR-positive animalsLDV infectionClinical presentationAxonal degenerationICR miceVentral rootsTypical neuropathologyTransplantable tumorsInadvertent exposurePoliomyelitisBasement membrane matrixHindlimb musculaturePremonitory signsDesigning Phenotyping Studies for Genetically Engineered Mice
Zeiss CJ, Ward JM, Allore HG. Designing Phenotyping Studies for Genetically Engineered Mice. Veterinary Pathology 2011, 49: 24-31. PMID: 21930803, PMCID: PMC3957214, DOI: 10.1177/0300985811417247.Peer-Reviewed Original ResearchMaropitant 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 resultsEndocytosisProgressive aggregation despite chaperone associations of a mutant SOD1-YFP in transgenic mice that develop ALS
Wang J, Farr GW, Zeiss CJ, Rodriguez-Gil DJ, Wilson JH, Furtak K, Rutkowski DT, Kaufman RJ, Ruse CI, Yates JR, Perrin S, Feany MB, Horwich AL. Progressive aggregation despite chaperone associations of a mutant SOD1-YFP in transgenic mice that develop ALS. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 1392-1397. PMID: 19171884, PMCID: PMC2631083, DOI: 10.1073/pnas.0813045106.Peer-Reviewed Original ResearchConceptsNucleotide exchange factorsIntermediate filament proteinsAbundant cytosolic enzymeChaperone interactionsExchange factorMutant formsAmyotrophic lateral sclerosis resultsChaperone associationMotor neuronsRNA hybridizationTransgenic animalsPunctate aggregatesSuperoxide dismutase 1Filament proteinsCytosolic enzymeMisfolded monomersHuman SOD1Predominant expressionSoluble stateBiochemical analysisInsoluble inclusionsDismutase 1Immunoaffinity captureProteinTransgenic miceEnhanced Ovarian Cancer Tumorigenesis and Metastasis by the Macrophage Colony-Stimulating Factor
Toy EP, Azodi M, Folk NL, Zito CM, Zeiss CJ, Chambers SK. Enhanced Ovarian Cancer Tumorigenesis and Metastasis by the Macrophage Colony-Stimulating Factor. Neoplasia 2009, 11: 136-144. PMID: 19177198, PMCID: PMC2631138, DOI: 10.1593/neo.81150.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorCell AdhesionCell MovementCell Transformation, NeoplasticFemaleHumansMacrophage Colony-Stimulating FactorMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisNeoplasm TransplantationNeoplasms, ExperimentalOligonucleotides, AntisenseOvarian NeoplasmsPhenotypeReceptor, Macrophage Colony-Stimulating FactorTumor Cells, Cultured