2023
A Mouse Model of MHV‐1 Virus Infection for Study of Acute and Long COVID Infection
Masciarella A, Di Gregorio D, Ramamoorthy R, Hussain H, Jayakumar A, Paidas M. A Mouse Model of MHV‐1 Virus Infection for Study of Acute and Long COVID Infection. Current Protocols 2023, 3: e896. PMID: 37867460, PMCID: PMC10606938, DOI: 10.1002/cpz1.896.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCOVID-19Disease Models, AnimalHumansMiceMice, Inbred StrainsMice, TransgenicMurine hepatitis virusPost-Acute COVID-19 SyndromeSARS-CoV-2ConceptsSARS-CoV-2Pathological changesMouse modelTransgenic miceLong-term organ dysfunctionSARS-CoV-2 pathophysiologyIrreversible neurological complicationsPotential therapeutic interventionsAvailable human dataBiosafety level 2 laboratoryNon-human primatesBiosafety level 3 laboratoryNeurological complicationsOrgan dysfunctionAcute stageClinical symptomsLong-term effectsSevere casesClinical observationsViral infectionTherapeutic interventionsMHV-1Animal preparationsWeight lossBSL-3 laboratorySemi-natural housing rescues social behavior and reduces repetitive exploratory behavior of BTBR autistic-like mice
Binder M, Bordey A. Semi-natural housing rescues social behavior and reduces repetitive exploratory behavior of BTBR autistic-like mice. Scientific Reports 2023, 13: 16260. PMID: 37758896, PMCID: PMC10533821, DOI: 10.1038/s41598-023-43558-0.Peer-Reviewed Original ResearchLoss of endothelial glucocorticoid receptor accelerates organ fibrosis in db/db mice
Srivastava S, Goodwin J. Loss of endothelial glucocorticoid receptor accelerates organ fibrosis in db/db mice. American Journal Of Physiology. Renal Physiology 2023, 325: f519-f526. PMID: 37589053, PMCID: PMC10639025, DOI: 10.1152/ajprenal.00105.2023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDiabetes Mellitus, Type 2Endothelial CellsMetforminMiceMice, Inbred StrainsReceptors, GlucocorticoidConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorOrgan fibrosisMouse modelMultiple organsSpontaneous type 2 diabetesDb/db miceDiabetic kidney fibrosisReceptor-mediated upregulationUse of metforminDiabetic renal fibrosisType 2 diabetesMechanisms of fibrosisGenetic mouse modelsUpregulation of WntRenal fibrosisSevere fibrosisDb miceIL-6Key cytokineKidney fibrosisDisease processFibrosisFibrotic conditionsWnt inhibitorsA clinically relevant selective ERK-pathway inhibitor reverses core deficits in a mouse model of autism
Murari K, Abushaibah A, Rho J, Turner R, Cheng N. A clinically relevant selective ERK-pathway inhibitor reverses core deficits in a mouse model of autism. EBioMedicine 2023, 91: 104565. PMID: 37088035, PMCID: PMC10149189, DOI: 10.1016/j.ebiom.2023.104565.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutism Spectrum DisorderAutistic DisorderDisease Models, AnimalMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, Inbred StrainsConceptsMouse model of autismModel of idiopathic autismModel of autismAutism-like phenotypeAutism spectrum disorderPathophysiology of autismDevelopment of autism spectrum disorderCore deficitBTBR miceSubchronic treatmentBTBR modelRepetitive behaviorsSpectrum disorderERK pathwayIdiopathic autismAutismSyndromic autismTreating autismMouse modelAnimal modelsNeuronal densityC57BL/6J miceJuvenile miceBTBRInhibitor of ERK pathway
2022
Circadian Responses to Light in the BTBR Mouse
Shankara J, Horsley K, Cheng N, Rho J, Antle M. Circadian Responses to Light in the BTBR Mouse. Journal Of Biological Rhythms 2022, 37: 498-515. PMID: 35722987, PMCID: PMC9452857, DOI: 10.1177/07487304221102279.Peer-Reviewed Original ResearchConceptsBTBR T<sup>+</sup> Itpr3<sup>Autism spectrum disorderBTBR miceStudies of autism spectrum disorderDelayed sleep phase disorderSuprachiasmatic nucleusSleep phase disorderStrains of miceCircadian phenotypesBTBR modelCircadian problemsSpectrum disorderClinical populationsBTBRC57BL/6J controlsSleep fragmentationClinical conditionsPhase disorderLight cycleMiceExternal light cycleCircadian disruptionSleepLight-darkProfound sleep
2021
CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling
Qin L, Zhang H, Li B, Jiang Q, Lopez F, Min W, Zhou JH. CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling. Arteriosclerosis Thrombosis And Vascular Biology 2021, 41: 2943-2960. PMID: 34670407, PMCID: PMC8613000, DOI: 10.1161/atvbaha.121.316707.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsCells, CulturedEndothelial CellsEndothelium, LymphaticFemaleGene DeletionHemangioma, Cavernous, Central Nervous SystemHyperplasiaMaleMAP Kinase Signaling SystemMice, Inbred StrainsModels, AnimalNF-kappa BTranslocation, GeneticVascular Endothelial Growth Factor Receptor-3ConceptsLymphatic ECsLymphatic defectsCerebral cavernous malformationsPan-endothelial cellsGrowth factor receptorTranscriptional levelTransport assaysLymphatic hyperplasiaCCM genesLymphatic dysfunctionNuclear translocationGenesFactor receptorVEGFR3ERK1/2Nuclear factorDeletionEC proliferationInhibition of VEGFR3Dependent mannerVascular endothelial growth factor receptorEndothelial growth factor receptorEC deletionAbnormal valve structureKPNA2Somatic PIK3CA Mutations in Sporadic Cerebral Cavernous Malformations
Peyre M, Miyagishima D, Bielle F, Chapon F, Sierant M, Venot Q, Lerond J, Marijon P, Abi-Jaoude S, Le Van T, Labreche K, Houlston R, Faisant M, Clémenceau S, Boch AL, Nouet A, Carpentier A, Boetto J, Louvi A, Kalamarides M. Somatic PIK3CA Mutations in Sporadic Cerebral Cavernous Malformations. New England Journal Of Medicine 2021, 385: 996-1004. PMID: 34496175, PMCID: PMC8606022, DOI: 10.1056/nejmoa2100440.Peer-Reviewed Original ResearchConceptsSporadic cerebral cavernous malformationCerebral cavernous malformationsFamilial cerebral cavernous malformationsCavernous malformationsTissue samplesSomatic PIK3CA mutationsCentral nervous systemVascular malformationsPIK3CA mutationsMouse modelHarbored mutationsNervous systemPatientsHuman meningiomasMeningiomasCommon genetic driversGenetic causeLesion tissueMalformationsFunction mutationsSomatic mutationsGenetic driversMiceReaction analysisMutationsThe lysophospholipid‐binding molecule CD1D is not required for the alloimmunization response to fresh or stored RBCs in mice despite RBC storage driving alterations in lysophospholipids
Medved J, Knott BM, Tarrah SN, Li AN, Shah N, Moscovich TC, Boscia AR, Salazar JE, Santhanakrishnan M, Hendrickson JE, Fu X, Zimring JC, Luckey CJ. The lysophospholipid‐binding molecule CD1D is not required for the alloimmunization response to fresh or stored RBCs in mice despite RBC storage driving alterations in lysophospholipids. Transfusion 2021, 61: 2169-2178. PMID: 34181769, PMCID: PMC8856511, DOI: 10.1111/trf.16554.Peer-Reviewed Original ResearchMeSH KeywordsAlarminsAnimalsAntibody SpecificityAntigens, CD1dBlood PreservationBlood TransfusionDuffy Blood-Group SystemErythrocytesFemaleImmunizationImmunoglobulin GImmunoglobulin MIsoantibodiesIsoantigensLysophospholipidsMaleMass SpectrometryMiceMice, Inbred StrainsMice, KnockoutMice, TransgenicMuramidaseOvalbuminReceptors, Cell SurfaceTransfusion ReactionConceptsCD1d-deficient miceCD1d deficiencyRBC alloimmunizationImmune activationNonclassical major histocompatibility complex class IWild-type control miceMajor histocompatibility complex class IHistocompatibility complex class IAdverse clinical consequencesSignificant adverse clinical consequencesLow baseline levelsRBC storageComplex class IHOD RBCsMolecule CD1dRBC transfusionWT miceControl miceImmune responseClinical consequencesMouse modelCD1dCD1d recognitionPolyclonal immunoglobulinsBaseline levels
2020
CD300LF Polymorphisms of Inbred Mouse Strains Confer Resistance to Murine Norovirus Infection in a Cell Type-Dependent Manner
Furlong K, Biering SB, Choi J, Wilen CB, Orchard RC, Wobus CE, Nelson CA, Fremont DH, Baldridge MT, Randall G, Hwang S. CD300LF Polymorphisms of Inbred Mouse Strains Confer Resistance to Murine Norovirus Infection in a Cell Type-Dependent Manner. Journal Of Virology 2020, 94: 10.1128/jvi.00837-20. PMID: 32581099, PMCID: PMC7431780, DOI: 10.1128/jvi.00837-20.Peer-Reviewed Original ResearchConceptsBone marrow-derived macrophagesCell type-dependent mannerType-dependent mannerCell typesMacrophage-like cellsRobust experimental systemMNV infectionRelated murine norovirusSpecific cell typesCorresponding mutantsMarrow-derived macrophagesMurine norovirus infectionEntry factorsMurine norovirusCD300lfCause of gastroenteritisNonpermissive cellsProteinaceous receptorsConfer resistanceHuman cellsHost cellsDifferent allelesAmino acidsC57BL/6J allelePermissive cells
2019
In vivo Firre and Dxz4 deletion elucidates roles for autosomal gene regulation
Andergassen D, Smith ZD, Lewandowski JP, Gerhardinger C, Meissner A, Rinn JL. In vivo Firre and Dxz4 deletion elucidates roles for autosomal gene regulation. ELife 2019, 8: e47214. PMID: 31738164, PMCID: PMC6860989, DOI: 10.7554/elife.47214.Peer-Reviewed Original ResearchConceptsX-chromosome inactivationAutosomal gene regulationGene regulationDouble deletionOrgan-specific mannerChromosome inactivationGene setsX chromosomeTranscriptional effectsExpression signaturesLociCell linesDeletionGenesRegulationVivo contributionRecent evidenceMegadomainsAutosomesFIRREMutantsChromosomesMain driversBiologySuperloopsConcentration-dependent Toxicity after Subcutaneous Administration of Meloxicam to C57BL/6N Mice (Mus musculus).
Sarfaty AE, Zeiss CJ, Willis AD, Harris JM, Smith PC. Concentration-dependent Toxicity after Subcutaneous Administration of Meloxicam to C57BL/6N Mice (Mus musculus). Journal Of The American Association For Laboratory Animal Science 2019, 58: 802-809. PMID: 31540585, PMCID: PMC6926403, DOI: 10.30802/aalas-jaalas-19-000037.Peer-Reviewed Original ResearchConceptsInjection siteFull-thickness epidermal necrosisPost-operative analgesiaFemale C57BL/6N miceMouse Grimace ScaleYoung adult malesNSAID dosesGastrointestinal ulcerationCavitary lesionsC57BL/6N miceEpidermal necrosisKidney lesionsNSAID toxicityGastric ulcerationSaline controlsSubcutaneous administrationPathologic lesionsRelevant pathologyMinimal dosesLesionsSevere pathologySkin pathologyMiceSeventh dayMeloxicam
2018
Comorbid epilepsy in autism spectrum disorder: Implications of postnatal inflammation for brain excitability
Lewis M, Kesler M, Candy S, Rho J, Pittman Q. Comorbid epilepsy in autism spectrum disorder: Implications of postnatal inflammation for brain excitability. Epilepsia 2018, 59: 1316-1326. PMID: 29858515, DOI: 10.1111/epi.14440.Peer-Reviewed Original ResearchConceptsAdult BTBR miceAutism spectrum disorderBTBR miceCore behavioural characteristicsSpectrum disorderBehavioral characteristics of autism spectrum disorderCharacteristics of autism spectrum disorderPresentation of autism spectrum disorderConcurrent presentationFemale BTBR miceASD-like behaviorsBTBR T+ Itpr3tf/JHippocampal cytokine levelsPathogenesis of autism spectrum disorderPostnatal immune challengeBrain excitabilityPentylenetetrazol-induced seizuresSaline-treated controlsDorsal hippocampusMotor stereotypiesCommunication deficitsDevelopment of targeted therapiesPostnatal day (P)7Comorbid epilepsyTumor necrosis factor-aPRC1 Fine-tunes Gene Repression and Activation to Safeguard Skin Development and Stem Cell Specification
Cohen I, Zhao D, Bar C, Valdes VJ, Dauber-Decker KL, Nguyen MB, Nakayama M, Rendl M, Bickmore WA, Koseki H, Zheng D, Ezhkova E. PRC1 Fine-tunes Gene Repression and Activation to Safeguard Skin Development and Stem Cell Specification. Cell Stem Cell 2018, 22: 726-739.e7. PMID: 29727681, PMCID: PMC5944606, DOI: 10.1016/j.stem.2018.04.005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiocatalysisMiceMice, Inbred StrainsMice, KnockoutPolycomb Repressive Complex 1Polycomb Repressive Complex 2SkinStem CellsConceptsNon-canonical PRC1 complexesStem cell specificationPRC1 complexesCell specificationSkin developmentDiverse rolesRepressive Complex 1Essential chromatin regulatorsPrecise developmental programExpression of genesCanonical PRC1PRC1 bindsPRC1 functionChromatin regulatorsGene repressionActive genesCell identityRepressor functionDevelopmental programSC formationFurther dissectionGenesPRC2PRC1Function studies
2017
Fibroblast growth factor receptor is a mechanistic link between visceral adiposity and cancer
Chakraborty D, Benham V, Bullard B, Kearney T, Hsia HC, Gibbon D, Demireva EY, Lunt SY, Bernard JJ. Fibroblast growth factor receptor is a mechanistic link between visceral adiposity and cancer. Oncogene 2017, 36: 6668-6679. PMID: 28783178, PMCID: PMC5709202, DOI: 10.1038/onc.2017.278.Peer-Reviewed Original ResearchConceptsAdipose tissueFibroblast growth factor-2 levelsGrowth factor-2 levelsFGFR-1Cancer prevention strategiesEpithelial cellsExcess adipose tissueTumor formationFactor 2 levelsVisceral adipose tissueNovel ex vivo systemSkin tumor formationObese human donorsNon-tumorigenic epithelial cellsSoft agarEx vivo systemGrowth factor receptorAdjuvant therapyEpithelial cell growthVisceral adiposityLevels of FGF2Obese individualsEpidemiological evidenceFibroblast growth factor receptorCancer risk
2016
Outbred CD1 mice are as suitable as inbred C57BL/6J mice in performing social tasks
Hsieh LS, Wen JH, Miyares L, Lombroso PJ, Bordey A. Outbred CD1 mice are as suitable as inbred C57BL/6J mice in performing social tasks. Neuroscience Letters 2016, 637: 142-147. PMID: 27871995, PMCID: PMC5203811, DOI: 10.1016/j.neulet.2016.11.035.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutistic DisorderBehavior, AnimalDisease Models, AnimalExploratory BehaviorMaleMice, Inbred StrainsSocial BehaviorTask Performance and AnalysisConceptsOutbred CD1 miceC57 miceCD1 miceAge-matched male miceThree-chamber sociability testThree-chamber testThree-chamber taskStranger mouseSocial interaction testAggressive behaviorMale CD1C57BL/6J miceMale miceBehavioral testingSociability testOutbred miceMiceMouse strainsStatistical significanceInteraction testMore timeDisruption of visual circuit formation and refinement in a mouse model of autism
Cheng N, Khanbabaei M, Murari K, Rho J. Disruption of visual circuit formation and refinement in a mouse model of autism. Autism Research 2016, 10: 212-223. PMID: 27529416, PMCID: PMC5324550, DOI: 10.1002/aur.1687.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutism Spectrum DisorderDisease Models, AnimalGeniculate BodiesMaleMiceMice, Inbred StrainsMicroscopy, ConfocalOptic TractConceptsAutism spectrum disorderDorsal lateral geniculate nucleusBTBR miceMouse modelMouse models of autism spectrum disordersModel of autism spectrum disorderMouse model of autismPathophysiology of autism spectrum disorderPrimary process mechanismsModel of autismEye-specific segregationPatterns of synaptic connectivityNeuroimaging studiesBTBR TBTBR animalsAberrant connectivityNeural circuitrySpectrum disorderAutistic behaviorPersistent deficitsBTBRDisrupted connectivityAxonal refinementLateral geniculate nucleusNeonatal stageGenetic modifications associated with ketogenic diet treatment in the BTBRT+Tf/J mouse model of autism spectrum disorder
Mychasiuk R, Rho J. Genetic modifications associated with ketogenic diet treatment in the BTBRT+Tf/J mouse model of autism spectrum disorder. Autism Research 2016, 10: 456-471. PMID: 27529337, DOI: 10.1002/aur.1682.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutism Spectrum DisorderBrainDiet, KetogenicDisease Models, AnimalGene ExpressionHumansMaleMiceMice, Inbred StrainsRNA, MessengerConceptsAutism spectrum disorderMouse models of autism spectrum disordersModel of autism spectrum disorderBTBR miceSpectrum disorderImpairments associated with autism spectrum disorderBTBR mouse model of ASDKetogenic dietBTBR mouse modelASD-like behaviorsImpaired GABAergic transmissionHeterogeneous neurodevelopmental disorderWhite matter developmentTemporal cortexBehavioral phenotypesKetogenic diet treatmentBrain regionsBehavioral abnormalitiesGABAergic transmissionVitamin D pathwayNeurodevelopmental disordersSpectrum of disordersMyelin formationNeuroprotective dietsBTBRSexual dimorphism of liver metastasis by murine pancreatic neuroendocrine tumors is affected by expression of complement C5
Contractor T, Kobayashi S, da Silva E, Clausen R, Chan C, Vosburgh E, Tang LH, Levine AJ, Harris CR. Sexual dimorphism of liver metastasis by murine pancreatic neuroendocrine tumors is affected by expression of complement C5. Oncotarget 2016, 7: 30585-30596. PMID: 27105526, PMCID: PMC5058703, DOI: 10.18632/oncotarget.8874.Peer-Reviewed Original ResearchConceptsComplement C5Liver metastasesAdvanced tumorsNeuroendocrine tumorsMouse modelSmall primary tumorsPancreatic neuroendocrine tumorsTypes of tumorsSmall molecule antagonistsIntratumoral levelsPrimary tumorMale miceComplement C5aMetastasisTumorsMolecule antagonistsMiceHigh frequencySexual dimorphismHuman diseasesMalesFirst reportCD88CD68PMX53Ketogenic diet restores aberrant cortical motor maps and excitation-to-inhibition imbalance in the BTBR mouse model of autism spectrum disorder
Smith J, Rho J, Teskey G. Ketogenic diet restores aberrant cortical motor maps and excitation-to-inhibition imbalance in the BTBR mouse model of autism spectrum disorder. Behavioural Brain Research 2016, 304: 67-70. PMID: 26876011, DOI: 10.1016/j.bbr.2016.02.015.Peer-Reviewed Original ResearchConceptsAutism spectrum disorderMouse models of autism spectrum disordersModel of autism spectrum disorderSpectrum disorderBTBR mouse model of ASDBTBR mouse modelPathophysiology of autism spectrum disorderRepetitive motor behaviorsKetogenic dietBalance of excitation/inhibitionCortical excitation/inhibition balanceHigh-resolution intracortical microstimulationBTBR miceBalance of excitationAutistic behaviorSensory processingMotor behaviorBTBRExcitation/inhibition balanceNeurodevelopmental disordersIncreased neuronal excitabilityLow-carbohydrate ketogenic dietMotor mappingDisordersRodent models
2015
Evidence of CNIH3 involvement in opioid dependence
Nelson EC, Agrawal A, Heath AC, Bogdan R, Sherva R, Zhang B, Al-Hasani R, Bruchas MR, Chou YL, Demers CH, Carey CE, Conley ED, Fakira AK, Farrer LA, Goate A, Gordon S, Henders AK, Hesselbrock V, Kapoor M, Lynskey MT, Madden PA, Moron JA, Rice JP, Saccone NL, Schwab SG, Shand FL, Todorov AA, Wallace L, Wang T, Wray NR, Zhou X, Degenhardt L, Martin NG, Hariri AR, Kranzler HR, Gelernter J, Bierut LJ, Clark DJ, Montgomery GW. Evidence of CNIH3 involvement in opioid dependence. Molecular Psychiatry 2015, 21: 608-614. PMID: 26239289, PMCID: PMC4740268, DOI: 10.1038/mp.2015.102.Peer-Reviewed Original ResearchConceptsSingle nucleotide polymorphismsGenome-wide association studiesComputational genetic analysisEpigenetic annotationsGenetic analysisAssociation studiesGenetic studiesStudy of AddictionVivo functionalityMouse strainsOpioid dependenceNeurogenetics StudySevere addictive disordersΑ-aminoGenesOpioid misusersGeneticsCnih3SNPsDuke Neurogenetics StudyHaplotypesPhenotypeA alleleAllelesFetal brain
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