Search results for "Mouse"

showing 10 items of 590 documents

High Fructose Diet inducing diabetes rapidly impacts olfactory epithelium and behavior in mice

2016

AbstractType 2 Diabetes (T2D), a major public health issue reaching worldwide epidemic, has been correlated with lower olfactory abilities in humans. As olfaction represents a major component of feeding behavior, its alteration may have drastic consequences on feeding behaviors that may in turn aggravates T2D. In order to decipher the impact of T2D on the olfactory epithelium, we fed mice with a high fructose diet (HFruD) inducing early diabetic state in 4 to 8 weeks. After only 4 weeks of this diet, mice exhibited a dramatic decrease in olfactory behavioral capacities. Consistently, this decline in olfactory behavior was correlated to decreased electrophysiological responses of olfactory n…

0301 basic medicineOlfactory systemmedicine.medical_specialtyolfaction;fructose;diabete;physiology;behavior;mouseinjuryPopulationType 2 diabetesOlfactionBiologysystemleptinArticleinsulin-resistance03 medical and health sciencescardiac-hypertrophyneuropeptide-y0302 clinical medicineInsulin resistance[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyInternal medicineDiabetes mellitusmedicineFood and Nutritioneducationmarker proteineducation.field_of_studyMultidisciplinaryLeptinNeurosciencesapoptosismedicine.disease3. Good health030104 developmental biologyEndocrinologymedicine.anatomical_structuresensory neuronsNeurons and CognitionAlimentation et NutritionOlfactory epithelium030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologymellitus
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A free radical theory of frailty.

2018

The free radical theory of ageing provided an intellectual framework for many laboratories working on ageing. However, experimental and clinical evidence showing that high doses of antioxidants do not have an effect on ageing or on age-associated diseases, cast doubts on the validity of this theory. Data from our own laboratory show that oxidative damage does not correlate with age, especially in the geriatric population, but rather with the frailty state. This has led us to postulate the free radical theory of frailty that proposes that oxidative damage is associated with frailty, but not with chronological age itself. Superoxide dismutase deficient mice are more frail than controls. But m…

0301 basic medicineOncologymedicine.medical_specialtyAgingFree Radicalsmedicine.disease_causeBiochemistrySuperoxide dismutase03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicineDeficient mouseHigh dosesMedicineAnimalsHumansFree-radical theory of agingGeriatricsbiologyFrailtybusiness.industryChronological ageOxidative Stress030104 developmental biologyAgeingbiology.proteinbusiness030217 neurology & neurosurgeryOxidative stressFree radical biologymedicine
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A conditional inducible JAK2V617F transgenic mouse model reveals myeloproliferative disease that is reversible upon switching off transgene expressio…

2019

Aberrant activation of the JAK/STAT pathway is thought to be the critical event in the pathogenesis of the chronic myeloproliferative neoplasms, polycythemia vera, essential thrombocythemia and primary myelofibrosis. The most frequent genetic alteration in these pathologies is the activating JAK2V617F mutation, and expression of the mutant gene in mouse models was shown to cause a phenotype resembling the human diseases. Given the body of genetic evidence, it has come as a sobering finding that JAK inhibitor therapy only modestly suppresses the JAK2V617F allele burden, despite showing clear benefits in terms of reducing splenomegaly and constitutional symptoms in patients. To gain a better …

0301 basic medicinePhysiologyClone (cell biology)Mice0302 clinical medicineAnimal CellsBone MarrowImmune PhysiologyMedicine and Health SciencesBlood and Lymphatic System ProceduresTransgenesBone Marrow TransplantationRegulation of gene expressionMultidisciplinaryQRAnimal ModelsBody FluidsPhenotypesBloodExperimental Organism Systems030220 oncology & carcinogenesisMedicineAnatomyCellular TypesResearch ArticleGenetically modified mousePlateletsTransgeneScienceImmunologyMutation MissenseMice TransgenicMouse ModelsSurgical and Invasive Medical ProceduresBone Marrow CellsBiologyResearch and Analysis Methods03 medical and health sciencesModel OrganismsmedicineGeneticsAnimalsHumansAlleleProgenitor cellMyelofibrosisMolecular Biology TechniquesMolecular BiologyTransplantationMyeloproliferative DisordersBlood CellsEssential thrombocythemiaBiology and Life SciencesCell BiologyJanus Kinase 2medicine.diseaseHematopoietic Stem CellsDisease Models Animal030104 developmental biologyAmino Acid SubstitutionGene Expression RegulationImmune SystemCancer researchAnimal StudiesSpleenCloningPLoS ONE
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Activin Receptor Ligand Blocking and Cancer Have Distinct Effects on Protein and Redox Homeostasis in Skeletal Muscle and Liver

2019

Muscle wasting in cancer cachexia can be alleviated by blocking activin receptor type 2 (ACVR2) ligands through changes in protein synthesis/degradation. These changes in cellular and protein metabolism may alter protein homeostasis. First, we elucidated the acute (1–2 days) and 2-week effects of blocking ACVR2 ligands by soluble activin receptor 2B (sACVR2B-Fc) on unfolded protein response (UPR), heat shock proteins (HSPs) and redox balance in a healthy mouse skeletal muscle. Second, we examined UPR, autophagy and redox balance with or without sACVR2B-Fc administration in muscle and liver of C26 tumor-bearing mice. The indicators of UPR and HSPs were not altered 1–2 days after a single sAC…

0301 basic medicinePhysiologyProtein metabolismlihaksetMyostatinlcsh:PhysiologyMuscle hypertrophyACTIVATIONchemistry.chemical_compound0302 clinical medicineENDOPLASMIC-RETICULUM STRESSCACHEXIAglutathioneta315Original ResearchIIB RECEPTORbiologylcsh:QP1-981Chemistry1184 Genetics developmental biology physiologyactivinActivin receptorMOUSE MODELunfolded protein response3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesismyostatinsyöpätauditautofagiacancer cachexiamedicine.medical_specialtyendocrine systemautophagyoxidative stress/redoxta3111liverCachexia03 medical and health sciencesPhysiology (medical)Internal medicinemedicineHEAT-SHOCK PROTEINSskeletal muscleglutationioksidatiivinen stressiECCENTRIC EXERCISEmaksaSkeletal muscleGlutathionemedicine.diseaseMUSCULAR-DYSTROPHY030104 developmental biologyEndocrinologybiology.proteinOXIDATIVE DAMAGE3111 BiomedicineproteiinitlihassurkastumasairaudetACVR2BFrontiers in Physiology
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Frontiers in Physiology

2021

Besides its roles in locomotion and thermogenesis, skeletal muscle plays a significant role in global glucose metabolism and insulin sensitivity through complex nutrient sensing networks. Our previous work showed that the muscle-specific ablation of O-GlcNAc transferase (OGT) led to a lean phenotype through enhanced interleukin-15 (IL-15) expression. We also showed OGT epigenetically modified and repressed the Il15 promoter. However, whether there is a causal relationship between OGT ablation-induced IL-15 secretion and the lean phenotype remains unknown. To address this question, we generated muscle specific OGT and interleukin-15 receptor alpha subunit (IL-15rα) double knockout mice (mDKO…

0301 basic medicinePhysiologymyokinesinterleukin-15Nutrient sensingCarbohydrate metabolism03 medical and health sciences0302 clinical medicinetissue cross-talkPhysiology (medical)Myokinemedicineinsulin sensitivityQP1-981ReceptorG alpha subunitChemistrySkeletal muscleBrief Research ReportCell biology030104 developmental biologymedicine.anatomical_structureKnockout mouseO-GlcNAc signalingSignal transduction030217 neurology & neurosurgeryFrontiers in Physiology
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Small Rab GTPases in Intracellular Vesicle Trafficking: The Case of Rab3A/Raphillin-3A Complex in the Kidney

2021

Small Rab GTPases, the largest group of small monomeric GTPases, regulate vesicle trafficking in cells, which are integral to many cellular processes. Their role in neurological diseases, such as cancer and inflammation have been extensively studied, but their implication in kidney disease has not been researched in depth. Rab3a and its effector Rabphillin-3A (Rph3A) expression have been demonstrated to be present in the podocytes of normal kidneys of mice rats and humans, around vesicles contained in the foot processes, and they are overexpressed in diseases with proteinuria. In addition, the Rab3A knockout mice model induced profound cytoskeletal changes in podocytes of high glucose fed a…

0301 basic medicineQH301-705.5Kidney Glomerulus030232 urology & nephrologyVesicular Transport ProteinsNerve Tissue ProteinsGTPaseReviewBiologyKidneyRabphilin-3ACatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryBiology (General)CytoskeletonMolecular BiologyQD1-999SpectroscopyAdaptor Proteins Signal TransducingKidneyEffectorPodocytesVesicleOrganic ChemistryRab3AIntracellular vesicleEpithelial CellsGeneral Medicinerab3A GTP-Binding ProteinComputer Science ApplicationsCell biologyChemistry030104 developmental biologymedicine.anatomical_structurerab GTP-Binding ProteinsRab proteinsKnockout mouseRabInternational Journal of Molecular Sciences
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The actin remodeling protein cofilin is crucial for thymic αβ but not γδ T-cell development

2018

Cofilin is an essential actin remodeling protein promoting depolymerization and severing of actin filaments. To address the relevance of cofilin for the development and function of T cells in vivo, we generated knock-in mice in which T-cell–specific nonfunctional (nf) cofilin was expressed instead of wild-type (WT) cofilin. Nf cofilin mice lacked peripheral αβ T cells and showed a severe thymus atrophy. This was caused by an early developmental arrest of thymocytes at the double negative (DN) stage. Importantly, even though DN thymocytes expressed the TCRβ chain intracellularly, they completely lacked TCRβ surface expression. In contrast, nf cofilin mice possessed normal numbers of γδ T cel…

0301 basic medicineReceptors Antigen T-Cell alpha-betaT-LymphocytesJurkat cellsenvironment and public healthImmune ReceptorsBiochemistryWhite Blood CellsJurkat CellsMice0302 clinical medicineContractile ProteinsSpectrum Analysis TechniquesShort ReportsAnimal CellsCell MovementT-Lymphocyte SubsetsMedicine and Health SciencesGene Knock-In TechniquesBiology (General)Post-Translational ModificationPhosphorylationThymocytesImmune System ProteinsT CellsGeneral NeuroscienceStem CellsReceptors Antigen T-Cell gamma-deltaTransfectionAnimal ModelsCofilinFlow CytometryCell biologyThymusmedicine.anatomical_structureExperimental Organism SystemsActin Depolymerizing FactorsSpectrophotometry030220 oncology & carcinogenesisPhosphorylationCytophotometryCellular TypesGeneral Agricultural and Biological SciencesSignal TransductionHematopoietic Progenitor CellsProlineQH301-705.5T cellImmune CellsImmunologyDouble negativeMouse Modelsmacromolecular substancesThymus GlandBiologyResearch and Analysis MethodsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesModel OrganismsmedicineAnimalsHumansActinBlood CellsGeneral Immunology and MicrobiologyActin remodelingBiology and Life SciencesProteinsCell BiologyActinsT Cell ReceptorsCytoskeletal Proteins030104 developmental biologyImmune SystemMutationPLoS Biology
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Rev-Erb modulates retinal visual processing and behavioral responses to light

2016

International audience; The circadian clock is thought to adjust retinal sensitivity to ambient light levels, yet the involvement of specific clock genes is poorly understood. We explored the potential role of the nuclear receptor subfamily 1, group D, member 1 (REV-ERB; or NR1D1) in this respect. In light-evoked behavioral tests, compared with wild-type littermates, Rev-Erb(-/-) mice showed enhanced negative masking at low light levels (0.1 lx). Rev-Erb(-/-) mouse retinas displayed significantly higher numbers of intrinsically photosensitive retinal ganglion cells (ipRGCs; 62% more compared with wild-type) and more intense melanopsin immunostaining of individual ipRGCs. In agreement with a…

0301 basic medicineRetinal Ganglion CellsLight[SDV]Life Sciences [q-bio]Circadian clockelectroretinogramBiochemistrychemistry.chemical_compound0302 clinical medicinecircadian clockskin and connective tissue diseasesComputingMilieux_MISCELLANEOUSMice KnockoutipRGCsBehavior AnimalphotoreceptorsorganizationCircadian Rhythmmedicine.anatomical_structurerodtranscriptionBiotechnologyPhotopic visionMelanopsinnegative maskingrat retinaBiologyRetina03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyCircadian ClocksGeneticsmedicineAnimalsCircadian rhythmScotopic visionmelanopsin-knockout miceMolecular BiologymouseRetinaIntrinsically photosensitive retinal ganglion cellsRod OpsinsRetinalganglion-cellsbody regionsmammalian retina030104 developmental biologychemistryNuclear Receptor Subfamily 1 Group D Member 1sense organsNeuroscience030217 neurology & neurosurgeryPhotic Stimulation[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Progressive Characterization of Visual Phenotype in Bardet-Biedl Syndrome Mutant Mice

2019

Purpose Bardet-Biedl syndrome (BBS) is an archetypical ciliopathy caused by defective ciliary trafficking and consequent function. Insights gained from BBS mouse models are applicable to other syndromic and nonsyndromic retinal diseases. This progressive characterization of the visual phenotype in three BBS mouse models sets a baseline for testing therapeutic interventions. Methods Longitudinal acquisition of electroretinograms, optical coherence tomography scans, and visual acuity using the optomotor reflex in Bbs6/Mkks, Bbs8/Ttc8, and Bbs5 knockout mice. Gene and protein expression analysis in vivo and in vitro. Results Complete loss of BBS5, BBS6, or BBS8 leads to different rates of reti…

0301 basic medicineRetinal degenerationAgingBBSomeGenotyping Techniquesgenetic structuresBlotting WesternGroup II ChaperoninsBBS5030105 genetics & heredityBiologyReal-Time Polymerase Chain ReactionRetinaMKKSMice03 medical and health sciencesBardet–Biedl syndromeElectroretinographymedicineAnimalsBardet-Biedl SyndromeVision OcularMice Knockoutmedicine.diagnostic_testRetinal DegenerationPhosphate-Binding Proteinsmedicine.diseaseImmunohistochemistryMice Mutant StrainsCytoskeletal ProteinsDisease Models AnimalCiliopathyPhenotype030104 developmental biologyKnockout mouseCarrier ProteinsMicrotubule-Associated ProteinsNeuroscienceTomography Optical CoherenceSignal TransductionElectroretinographyInvestigative Opthalmology & Visual Science
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Generation of an inducible RPE-specific Cre transgenic-mouse line.

2018

The retinal pigment epithelium (RPE) is an epithelial monolayer in the back of the vertebrate eye. RPE dysfunction is associated with retinal degeneration and blindness. In order to fully understand how dysregulation affects visual function, RPE-specific gene knockouts are indispensable. Since the currently available RPE-specific Cre recombinases show lack of specificity or poor recombination, we sought to generate an alternative. We generated a tamoxifen-inducible RPE-specific Cre transgenic mouse line under transcriptional control of an RPE-specific Tyrosinase enhancer. We characterized the Cre-mediated recombinant expression by crossing our RPE-Tyrosinase-CreErT2 mouse line with the tdTo…

0301 basic medicineRetinal degenerationMaleEmbryologylcsh:MedicineGene ExpressionRetinal Pigment EpitheliumBiochemistry0302 clinical medicineRecombinaseMedicine and Health Scienceslcsh:ScienceStainingMultidisciplinaryMonophenol MonooxygenaseAnimal ModelsSpecimen preparation and treatmentCell biologyEnzymesmedicine.anatomical_structureExperimental Organism SystemsModels AnimalFemaleAnatomyResearch ArticleGenetically modified mouseImaging TechniquesTransgeneOcular AnatomyMice TransgenicMouse ModelsBiologyResearch and Analysis MethodsRetinaRecombinases03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineGeneticsAnimalsEnhancerGene knockoutRetinaRetinal pigment epitheliumIntegraseslcsh:REmbryosDAPI stainingBiology and Life SciencesProteinsmedicine.diseaseeye diseasesMice Inbred C57BLLuminescent Proteins030104 developmental biologyNuclear stainingEnzymologyAnimal StudiesEyeslcsh:Qsense organsHead030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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