Search results for "mice"

showing 10 items of 6027 documents

Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer's Disease-Like Pathophysiology in APP/PS1 Mice.

2019

Glutamate excitotoxicity has long been related to Alzheimer's disease (AD) pathophysiology, and it has been shown to affect the major AD-related hallmarks, amyloid-β peptide (Aβ) accumulation and tau phosphorylation (p-tau). We investigated whether oral administration of monosodium glutamate (MSG) has effects in a murine model of AD, the double transgenic mice APP/PS1. We found that AD pathogenic factors appear earlier in APP/PS1 when supplemented with MSG, while wildtype mice were essentially not affected. Aβ and p-tau levels were increased in the hippocampus in young APP/PS1 animals upon MSG administration. This was correlated with increased Cdk5-p25 levels. Furthermore, in these mice, we…

0301 basic medicineGenetically modified mouseMalemedicine.medical_specialtyMonosodium glutamateExcitotoxicityHippocampusAdministration OralMice TransgenicAMPA receptormedicine.disease_cause03 medical and health scienceschemistry.chemical_compoundAmyloid beta-Protein PrecursorMice0302 clinical medicineOral administrationAlzheimer DiseaseInternal medicinemental disordersSodium GlutamatemedicinePresenilin-1Animalsbusiness.industryGeneral NeuroscienceGlutamate receptorLong-term potentiationGeneral MedicineFlavoring AgentsPsychiatry and Mental healthClinical Psychology030104 developmental biologyEndocrinologychemistryFemaleGeriatrics and Gerontologybusiness030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Cytoskeletal transgelin 2 contributes to gender-dependent adipose tissue expandability and immune function

2019

During adipogenesis, preadipocytes' cytoskeleton reorganizes in parallel with lipid accumulation. Failure to do so may impact the ability of adipose tissue (AT) to shift between lipid storage and mobilization. Here, we identify cytoskeletal transgelin 2 (TAGLN2) as a protein expressed in AT and associated with obesity and inflammation, being normalized upon weight loss. TAGLN2 was primarily found in the adipose stromovascular cell fraction, but inflammation, TGF-β, and estradiol also prompted increased expression in human adipocytes. Tagln2 knockdown revealed a key functional role, being required for proliferation and differentiation of fat cells, whereas transgenic mice overexpressing Tagl…

0301 basic medicineGenetically modified mouseMalemedicine.medical_specialtyTHP-1 CellsBlotting WesternAdipose tissueMuscle ProteinsInflammationMice TransgenicDiet High-FatBiochemistry03 medical and health sciencesMice0302 clinical medicineImmune systemSex FactorsInternal medicineGeneticsmedicineAdipocytesAnimalsHumansObesityadipocyte protein 2CytoskeletonMolecular BiologyCytoskeletonInflammationbiologyMicrofilament ProteinsPhenotypeImmunohistochemistryMice Inbred C57BL030104 developmental biologyEndocrinologyAdipose TissueAdipogenesisbiology.proteinFemalemedicine.symptom030217 neurology & neurosurgeryBiotechnology
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Gradual development of psoriatic skin lesions by constitutive low-level expression of IL-17A

2016

Psoriasis is a common chronic inflammatory skin disease restricted to humans. The understanding of its pathogenesis has long been hampered by the lack of suitable chronic mouse models. The cytokine IL-17A has emerged as a key player in epithelial immune responses and the defense against extracellular pathogens. Moreover, enhanced expression of IL-17A can turn pathologic and is closely associated with psoriasis. In this study, we generated a novel transgenic mouse model that recapitulates many characteristics of psoriasis. DC-1L-17A(ind) mice with constitutive low-level expression of IL-17A by CD11c(+) cells gradually develop skin lesions during adult life. The lesions preferentially occur a…

0301 basic medicineGenetically modified mousemedicine.medical_treatmentImmunologyCD11cInflammationAnimals Genetically ModifiedPathogenesisMice03 medical and health sciences0302 clinical medicineImmune systemSDG 3 - Good Health and Well-beingPsoriasismedicineAnimalsHumansPsoriasisCells CulturedSkinbusiness.industryInterleukin-17Dendritic Cellsmedicine.diseaseCD11c AntigenDisease Models Animal030104 developmental biologyCytokineImmunologyCytokinesInterleukin 17medicine.symptombusiness030215 immunologyCellular Immunology
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Wnt-Dependent Oligodendroglial-Endothelial Interactions Regulate White Matter Vascularization and Attenuate Injury

2020

Recent studies have indicated oligodendroglial-vascular crosstalk during brain development, but the underlying mechanisms are incompletely understood. We report that oligodendrocyte precursor cells (OPCs) contact sprouting endothelial tip cells in mouse, ferret and human neonatal white matter. Using transgenic mice, we show that increased or decreased OPC density results in cognate changes in white matter vascular investment. Hypoxia promoted both increased OPC numbers and higher white matter vessel density, and endothelial cell expression of the Wnt pathway targets Apcdd1 and Axin2, suggesting paracrine OPC-endothelial signaling. Conditional knockout of OPC Wntless resulted in diminished w…

0301 basic medicineGenetically modified mouseoligodendrocytesMice TransgenicBiologyArticleWhite matter03 medical and health sciencesParacrine signallingMice0302 clinical medicinetip cell angiogenesisAxin ProteinConditional gene knockoutmedicineAXIN2AnimalsHumanshypoxic-ischemic encephalopathyHypoxiaWnt Signaling PathwayGeneral NeuroscienceWnt signaling pathwayFerretsIntracellular Signaling Peptides and ProteinsEndothelial CellsMembrane ProteinsCell DifferentiationHypoxia (medical)Wnt signalingWhite Matter3. Good healthCell biologyEndothelial stem cellstomatognathic diseasesOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemEndothelium Vascularmedicine.symptom030217 neurology & neurosurgeryNeuron
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Whole genome sequences reveal Vibrio hemicentroti Kim et al. 2013 as a later heterotypic synonym of Vibrio splendidus (Beijerinck 1900) Baumann et al…

2017

The synonymy between Vibrio hemicentroti Kim et al. 2013 and Vibrio splendidus (Beijerinck 1900) Baumann et al. 1981 was suggested after a recent multilocus sequence analysis of the Splendidus clade, which included the type strains of both species. To clarify their status, we have determined genomic indexes from whole genome sequences of strains V. hemicentroti CECT 8714T and V. splendidus NCCB 53037T. Average Nucleotide Identities of 96.0–96.7 % and an in silico DNA–DNA hybridization value of 70.2 %, as well as similarity levels of selected housekeeping gene sequences support the consideration of V. hemicentroti as a later heterotypic synonym of V. splendidus .

0301 basic medicineGeneticsDNA BacterialSynonymSequence analysisNucleic Acid HybridizationGeneral MedicineVibrio hemicentrotiSequence Analysis DNABiologyMicrobiologyGenomeMicrobiologyHousekeeping geneBacterial Typing Techniques03 medical and health sciences030104 developmental biologyVibrio splendidusCladeEcology Evolution Behavior and SystematicsPhylogenyMultilocus Sequence TypingVibrioInternational journal of systematic and evolutionary microbiology
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DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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With mouse age comes wisdom : a review and suggestions of relevant mouse models for age-related conditions

2016

Ageing is a complex multifactorial process that results in many changes in physiological changes processes that ultimately increase susceptibility to a wide range of diseases. As such an ageing population is resulting in a pressing need for more and improved treatments across an assortment of diseases. Such treatments can come from a better understanding of the pathogenic pathways which, in turn, can be derived from models of disease. Therefore the more closely the model resembles the disease situation the more likely relevant the data will be that is generated from them. Here we review the state of knowledge of mouse models of a range of diseases and aspects of an ageing physiology that ar…

0301 basic medicineGerontologyAgingPopulation ageingProcess (engineering)TRAUMATIC BRAIN-INJURYDiseaseBiologyMouse modelsMice03 medical and health sciences0302 clinical medicineAge relatedMedicine and Health SciencesAnimalsHumansCLOSED-BONE-FRACTURESENESCENCE-ACCELERATED MOUSEE-DEFICIENT MICECELL-MEDIATED-IMMUNITYTRIPLE-TRANSGENIC MODELBiology and Life SciencesNECROSIS-FACTOR-ALPHAAged patientsCell mediated immunityC-REACTIVE PROTEINACTIVATION IN-VIVODisease Models AnimalPatient populationAgeing030104 developmental biologyAgeingPhenotypingMouse models ; ageing ; phenotypingLONG-TERM POTENTIATION030217 neurology & neurosurgeryCognitive psychologyDevelopmental Biology
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Frailty Quantified by the "Valencia Score" as a Potential Predictor of Lifespan in Mice.

2017

The development of frailty scores suitable for mice and which resemble those used in the clinical scenario is of great importance to understand human frailty. The aim of the study was to determine an individual frailty score for each mouse at different ages and analyze the association between the frailty score and its lifespan. For this purpose, the "Valencia Score" for frailty was used. Thus, a longitudinal study in mice was performed analyzing weight loss, running time and speed, grip strength and motor coordination at the late-adult, mature and old ages (40, 56 and 80 weeks old, respectively). These parameters are equivalent to unintentional weight loss, poor endurance, slowness, weaknes…

0301 basic medicineGerontologyWeaknessLongitudinal studyAgingFrail ElderlyLongevityHealthy Aging03 medical and health sciencesGrip strengthMice0302 clinical medicineWeight lossWeight LossmedicineAnimalsHumansLongitudinal StudiesMaze LearningClinical scenarioGeriatric AssessmentAgedMice Inbred ICRFrailtyHand Strengthbusiness.industryLow activityAging PrematureRunning timeMotor coordination030104 developmental biologyPhenotypeModels AnimalPhysical EnduranceFemaleGeriatrics and Gerontologymedicine.symptombusiness030217 neurology & neurosurgeryThe journals of gerontology. Series A, Biological sciences and medical sciences
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