2020
Slc20a1/Pit1 and Slc20a2/Pit2 are essential for normal skeletal myofiber function and survival
Chande S, Caballero D, Ho BB, Fetene J, Serna J, Pesta D, Nasiri A, Jurczak M, Chavkin NW, Hernando N, Giachelli CM, Wagner CA, Zeiss C, Shulman GI, Bergwitz C. Slc20a1/Pit1 and Slc20a2/Pit2 are essential for normal skeletal myofiber function and survival. Scientific Reports 2020, 10: 3069. PMID: 32080237, PMCID: PMC7033257, DOI: 10.1038/s41598-020-59430-4.Peer-Reviewed Original ResearchConceptsHyp miceMuscle functionSkeletal muscleMyofiber functionNormal body weightSkeletal muscle atrophyGene dose-dependent reductionConditional knockout miceReduced oxygen consumption rateStimulation of AMP kinaseKnockout miceHypophosphatemic disordersMuscle atrophyERK1/2 activationGrip strengthConditional deletionHormonal changesLow bloodBody weightC2C12 myoblastsMiceFurther evaluationBlood phosphateDependent reductionAMP kinase
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
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 deletion
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
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
2008
Reversal of Blindness in Animal Models of Leber Congenital Amaurosis Using Optimized AAV2-mediated Gene Transfer
Bennicelli J, Wright JF, Komaromy A, Jacobs JB, Hauck B, Zelenaia O, Mingozzi F, Hui D, Chung D, Rex TS, Wei Z, Qu G, Zhou S, Zeiss C, Arruda VR, Acland GM, Dell'Osso LF, High KA, Maguire AM, Bennett J. Reversal of Blindness in Animal Models of Leber Congenital Amaurosis Using Optimized AAV2-mediated Gene Transfer. Molecular Therapy 2008, 16: 458-465. PMID: 18209734, PMCID: PMC2842085, DOI: 10.1038/sj.mt.6300389.Peer-Reviewed Original ResearchConceptsLeber congenital amaurosisAnimal modelsCongenital amaurosisReversal of blindnessRetinal pigment epithelium cellsWeeks of injectionPigment epithelium cellsRPE65 formDose of vectorAppropriate target cellsVisual acuityVisual deficitsHistopathologic analysisAdeno-associated virusERG responsesRPE65 mutationsSubretinal deliveryEpithelium cellsMutant miceMinimal toxicityProtein expressionTarget cellsPupillary responseElectroretinogramAmaurosis
2003
The Apoptosis-Necrosis Continuum: Insights from Genetically Altered Mice
Zeiss CJ. The Apoptosis-Necrosis Continuum: Insights from Genetically Altered Mice. Veterinary Pathology 2003, 40: 481-495. PMID: 12949404, DOI: 10.1354/vp.40-5-481.Peer-Reviewed Original ResearchConceptsCell death programApoptosis-inducing factorTissue-specific rolesCaspase-dependent mechanismCaspase-dependent apoptosisApoptosis-necrosis continuumAnimal developmentDeath programKey genesApoptotic effectorsApoptotic phenotypeRegulated processCaspase activationIntimate crosstalkApoptotic cascadeDependent effectorsHomeostatic pathwaysCell deathNecrotic onesBiochemical networksApoptosisPathologic stimuliBiochemical featuresMutant miceGenesPathogenesis of mouse hepatitis virus infection in gamma interferon-deficient mice is modulated by co-infection with Helicobacter hepaticus.
Compton SR, Ball-Goodrich LJ, Zeiss CJ, Johnson LK, Johnson EA, Macy JD. Pathogenesis of mouse hepatitis virus infection in gamma interferon-deficient mice is modulated by co-infection with Helicobacter hepaticus. Comparative Medicine 2003, 53: 197-206. PMID: 12784855.Peer-Reviewed Original ResearchConceptsIFN-gamma KO miceGamma interferon-deficient miceMouse hepatitis virusInterferon-deficient miceDevelopment of peritonitisKO miceH. hepaticusMultisystemic infectionHelicobacter hepaticusMouse hepatitis virus infectionHepatitis virus infectionAberrant immune responseSelf-limiting infectionMinimal pathologic changesMultifocal hepatic necrosisLater time pointsAcute necrotizingAcute peritonitisAcute phaseInflammatory lesionsImmunocompetent miceChronic infectionHepatic necrosisMHV infectionPathologic changes