Search results for " Transgenic"

showing 10 items of 522 documents

Cardiomyocyte proliferation prevents failure in pressure overload but not volume overload

2017

Induction of the cell cycle is emerging as an intervention to treat heart failure. Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cyclin D2 would be beneficial during hemodynamic overload. We induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2-expressing and WT mice. Although cyclin D2 expression dramatically improved survival following TAC, it did not confer a survival advantage to mice following aortocaval shunt. Cardiac function decreased following TAC in WT mice, but was preserved in cyclin D2-expressing mice. On the other hand, cardiac structure and function were compr…

0301 basic medicineCardiac function curvemedicine.medical_specialtyAortic DiseasesVolume overloadCardiomegalyMice TransgenicConstriction Pathologic030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCyclin D2FibrosisInternal medicinemedicineAnimalsCyclin D2Myocytes CardiacCell ProliferationCyclinHeart FailurePressure overloadbusiness.industryGeneral MedicineCell cyclemedicine.disease030104 developmental biologyEndocrinologyHeart failurebusinessResearch ArticleJournal of Clinical Investigation
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CD40/CD40L and Related Signaling Pathways in Cardiovascular Health and Disease—The Pros and Cons for Cardioprotection

2020

The CD40–CD40 ligand (CD40L) dyad represents a scientific and clinical field that has raised many controversies in the past and cannot be clearly defined as being an either beneficial or harmful pathway. Being crucially involved in physiological immunological processes as well as pathological inflammatory reactions, the signaling pathway has been recognized as a key player in the development of both autoimmune and cardiovascular disease. Even though the possibilities of a therapeutic approach to the dyad were recognized decades ago, due to unfortunate events, detailed in this review, pharmacological treatment targeting the dyad, especially in patients suffering from atherosclerosis, is not …

0301 basic medicineCardiovascular healthMice TransgenicInflammationReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular SystemCatalysisAutoimmune DiseasesInorganic Chemistrylcsh:ChemistryMice03 medical and health sciencesTherapeutic approach0302 clinical medicineRisk Factorscardiovascular diseaseDiabetes mellitusCD40AnimalsHumansMedicineGene SilencingCD40 AntigensPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyCardioprotectionClinical Trials as Topicbusiness.industryOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science Applications030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Cardiovascular DiseasesinflammationCd40 cd40lSignal transductionmedicine.symptomCD40 ligandatherosclerosisbusinessSignal TransductionInternational Journal of Molecular Sciences
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Chronic benzodiazepine treatment decreases spine density in cortical pyramidal neurons.

2015

The adult brain retains a substantial capacity for synaptic reorganization, which includes a wide range of modifications from molecular to structural plasticity. Previous reports have demonstrated that the structural remodeling of excitatory neurons seems to occur in parallel to changes in GABAergic neurotransmission. The function of neuronal inhibitory networks can be modified through GABAA receptors, which have a binding site for benzodiazepines (BZ). Although BZs are among the most prescribed drugs, is not known whether they modify the structure and connectivity of pyramidal neurons. In the present study we wish to elucidate the impact of a chronic treatment of 21 days with diazepam (2mg…

0301 basic medicineCingulate cortexMaleDendritic spineDendritic SpinesPrefrontal CortexMice TransgenicBiologyInhibitory postsynaptic potential03 medical and health sciences0302 clinical medicinePostsynaptic potentialAnimalsGABA-A Receptor AgonistsDiazepamBehavior AnimalDose-Response Relationship DrugGABAA receptorGeneral NeurosciencePyramidal Cellsfood and beveragesLong-term potentiation030104 developmental biologynervous systemExcitatory postsynaptic potentialGABAergicNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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The NG2 Protein Is Not Required for Glutamatergic Neuron-NG2 Cell Synaptic Signaling.

2014

NG2 glial cells (as from now NG2 cells) are unique in receiving synaptic input from neurons. However, the components regulating formation and maintenance of these neuron–glia synapses remain elusive. The transmembrane protein NG2 has been considered a potential mediator of synapse formation and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) clustering, because it contains 2 extracellular Laminin G/Neurexin/Sex Hormone-Binding Globulin domains, which in neurons are crucial for formation of transsynaptic neuroligin– neurexin complexes. NG2 is connected via Glutamate Receptor-Interacting Protein with GluA2/3-containing AMPARs, thereby possibly mediating receptor clus…

0301 basic medicineCognitive NeuroscienceNeurexinSynaptogenesisGlutamic AcidNeuroliginMice TransgenicBiologyNeurotransmissionHippocampusSynaptic Transmission03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePostsynaptic potentialAnimalsReceptors AMPAAntigensNeuronsMembrane Proteins030104 developmental biologynervous systemSynaptic plasticitySynapsesProteoglycansSynaptic signalingNeurosciencePostsynaptic densityNeuroglia030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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Regulatory T Cells in an Endogenous Mouse Lymphoma Recognize Specific Antigen Peptides and Contribute to Immune Escape.

2019

Abstract Foxp3+ regulatory T cells (Tregs) sustain immune homeostasis and may contribute to immune escape in malignant disease. As a prerequisite for developing immunologic approaches in cancer therapy, it is necessary to understand the ontogeny and the antigenic specificities of tumor-infiltrating Tregs. We addressed this question by using a λ-MYC transgenic mouse model of endogenously arising B-cell lymphoma, which mirrors key features of human Burkitt lymphoma. We show that Foxp3+ Tregs suppress antitumor responses in endogenous lymphoma. Ablation of Foxp3+ Tregs significantly delayed tumor development. The ratio of Treg to effector T cells was elevated in growing tumors, which could be …

0301 basic medicineGenetically modified mouseCancer ResearchLymphoma B-CellImmunologychemical and pharmacologic phenomenaMice TransgenicT-Lymphocytes RegulatoryEpitope03 medical and health sciences0302 clinical medicineAntigenCell Line TumorMHC class ImedicineAnimalsAntigensbiologyEffectorFOXP3hemic and immune systemsmedicine.diseaseLymphomaMice Inbred C57BL030104 developmental biologyTumor Escape030220 oncology & carcinogenesisCancer researchbiology.proteinTumor EscapePeptidesCancer immunology research
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Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

2016

Background Obesity has tremendous impact on the health systems. Its epigenetic bases are unclear. MacroH2A1 is a variant of histone H2A, present in two alternatively exon-spliced isoforms macroH2A1.1 and macroH2A1.2, regulating cell plasticity and proliferation, during pluripotency and tumorigenesis. Their role in adipose tissue plasticity is unknown. Results Here, we show evidence that macroH2A1.1 protein levels in the visceral adipose tissue of obese humans positively correlate with BMI, while macroH2A1.2 is nearly absent. We thus introduced a constitutive GFP-tagged transgene for macroH2A1.2 in mice, and we characterized their metabolic health upon being fed a standard chow diet or a hig…

0301 basic medicineGenetically modified mouseCyclin-Dependent Kinase Inhibitor p21macroh2a1.2TransgeneAdipose tissueAdipose tissueMice TransgenicBiologyCarbohydrate metabolismDiet High-FatBody Mass IndexCell LineHistones03 medical and health sciencesMiceHistone variantGeneticsAnimalsHumansInsulinEpigeneticsAdipose tissue Histone variants Obesity macroh2a1.2ObesityTranscription factorPancreasMolecular BiologyUncoupling Protein 1SkinHistone variantsAdipogenesisResearchCell DifferentiationGlucose Tolerance TestMolecular biologyCell biologyMice Inbred C57BL030104 developmental biologyPhenotypeLiverMetabolic EngineeringAdipogenesisDNA methylationAdipose tissue; Histone variants; macroh2a1.2; Obesity; Molecular Biology; Genetics
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Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation.

2017

Organ fibrosis is characterized by a chronic wound-healing response, with excess deposition of extracellular matrix components. Here, collagen type I represents the most abundant scar component and a primary target for antifibrotic therapies. Liver fibrosis can progress to cirrhosis and primary liver cancer, which are the major causes of liver related morbidity and mortality. However, a (pro-)collagen type I specific therapy remains difficult and its therapeutic abrogation may incur unwanted side effects. We therefore designed tetracycline-regulated procollagen alpha1(I) short hairpin (sh)RNA expressing mice that permit a highly efficient inducible knockdown of the procollagen alpha1(I) gen…

0301 basic medicineGenetically modified mouseLiver CirrhosisPathologymedicine.medical_specialtyCirrhosisInflammationMice TransgenicCollagen Type ISmall hairpin RNAExtracellular matrix03 medical and health sciencesMiceFibrosismedicineAnimalsRNA Small InterferingMolecular BiologyCells CulturedGene knockdownExtracellular Matrix ProteinsChemistryMouse Embryonic Stem CellsFibroblastsmedicine.diseaseProcollagen peptidaseDisease Models Animal030104 developmental biologyGene Expression RegulationGene Knockdown TechniquesCancer researchmedicine.symptomProcollagenMatrix biology : journal of the International Society for Matrix Biology
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Shifts in gut microbiota composition in an APP/PSS1 transgenic mouse model of Alzheimer's disease during lifespan.

2017

Alzheimer's disease (AD) is the most common form of dementia and one of the major causes of disability and dependency in older people. Accumulating evidences link gut microbiota with different diseases and its relationship with neurodegenerative diseases is becoming most intriguing. This study was aimed to compare the gut microbiota of transgenic APP/PS1 (TG) mice, a well‐established deterministic mouse model of AD, with their C57BL/6 wild‐type (WT) littermates. Faecal samples were collected from 3‐, 6‐ and 24‐month‐old mice and analysed by pyrosequencing of the V1–V3 region of the bacterial 16S rRNA genes. Bacterial profiles were similar in all young mice (3 months old), and started to div…

0301 basic medicineGenetically modified mouseMaleAgingRikenellaceaeTransgeneFirmicutesMice TransgenicDiseaseGut floraApplied Microbiology and Biotechnology03 medical and health sciencesMiceAlzheimer DiseaseRNA Ribosomal 16SProteobacteriamedicineDementiaIndicatorsAnimalsHumansNeuroinflammationMarkersbiologyIntestinal microbiologyBacteroidetesbiology.organism_classificationmedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLDisease Models Animal030104 developmental biologyAgeingImmunologyMicrobial structureDisease processesLetters in applied microbiology
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Behavioral fragmentation in the D1CT-7 mouse model of Tourette's syndrome.

2017

Aim The transgenic D1CT-7 mouse is one of the best-characterized animal models of Tourette's syndrome (TS), exhibiting spontaneous tic-like Head-Body Twitches (HBT) and deficits in sensorimotor gating. This study is aimed at evaluating the behavioral dynamics of these mutants and their potential relevance to TS. Methods The behavior of D1CT-7 and Wild Type littermates was firstly assessed by considering frequencies and durations. To detect recurrent real-time behavioral sequences, the multivariate T-pattern analysis was employed. Analyses of transition probabilities among behaviors further provided an overall picture of the behavioral dynamics. Results T-patterns and transition matrices rev…

0301 basic medicineGenetically modified mouseMaleCholera ToxinTransgeneTourette's syndromeMice Transgenictransition matriceBiologyMotor ActivityTourette syndromeOpen fieldStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineSniffingPhysiology (medical)medicineAnimalsPharmacology (medical)tic disorderGait Disorders NeurologicPharmacologyMice Inbred BALB CD1CT-7Behavior AnimalReceptors Dopamine D1Wild typeBehavioral patternT-pattern analysiOriginal Articlesmedicine.diseasePhenotypeDisease Models Animal030104 developmental biologyPsychiatry and Mental HealthMotor SkillsExploratory BehaviorNeuroscience030217 neurology & neurosurgeryTourette SyndromeCNS neurosciencetherapeutics
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Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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