Search results for "Transgenic"

showing 10 items of 552 documents

PGC-1α: a master gene that is hard to master

2012

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a transcriptional coactivator that favorably affects mitochondrial function. This concept is supported by an increasing amount of data including studies in PGC-1α gene-deleted mice, suggesting that PGC-1α is a rescue factor capable of boosting cell metabolism and promoting cell survival. However, this view has now been called into question by a recent study showing that adeno-associated virus-mediated PGC-1α overexpression causes overt cell degeneration in dopaminergic neurons. How is this to be understood, and can these seemingly conflicting findings tell us something about the role of PGC-1α in cell stress and in cont…

medicine.medical_specialtyModels NeurologicalSettore BIO/11 - Biologia MolecolareRNA-binding proteinBiologyMitochondrionSettore BIO/09 - FisiologiaMiceCellular and Molecular NeuroscienceHeat shock proteinInternal medicinemedicineAnimalsHomeostasisHumansReceptorMolecular BiologyTranscription factorHeat-Shock ProteinsMice KnockoutPharmacologyPGC-1α Mitochondria Dopaminergic neurons Transgenic animal Adenovirus Parkinson’s diseaseDopaminergic NeuronsDopaminergicRNA-Binding ProteinsParkinson DiseaseCell BiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaEndocrinologyCell metabolismNerve DegenerationTrans-ActivatorsMolecular MedicineNeuroscienceHomeostasisTranscription FactorsCellular and Molecular Life Sciences
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Genetic Deletion of JNK1 and JNK2 Aggravates the DSS-Induced Colitis in Mice

2007

The c-Jun N-terminal kinases (JNKs) are considered as novel targets for therapy of inflammatory bowel diseases (IBD). However, the relevant JNK isoforms have to be elucidated. Here, we analyze the individual contribution of the JNK1 and JNK2 isoforms in a dextran sulfate sodium (DSS) model of experimental colitis. JNK1 and JNK2 knockout mice (JNK1 ko, JNK2 ko) and their wild-type controls (WT1, WT2) received three cycles of DSS treatment, each consisting of 1.7% DSS for 5 days, followed by 5 days with water. Animals were daily evaluated by a disease activity index (DAI) comprising measurement of body weight, estimation of stool consistency, and test for occult blood/gross rectal bleeding. A…

medicine.medical_specialtyPathologyCryptApoptosisMice TransgenicInflammatory bowel diseaseGastroenterologyProinflammatory cytokineMiceCecumImmune systemInternal medicineWeight LossAnimalsMitogen-Activated Protein Kinase 9MedicineMitogen-Activated Protein Kinase 8Single-Blind MethodIntestinal MucosaColitisCrosses Geneticbusiness.industryDextran SulfateColitismedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisChronic DiseaseKnockout mouseSurgeryGastrointestinal HemorrhagebusinessJournal of Investigative Surgery
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Restoration of cerebral and systemic microvascular architecture in APP/PS1 transgenic mice following treatment with Liraglutide™.

2015

OBJECTIVE: Cerebral microvascular impairments occurring in AD may reduce Aβ peptide clearance and impact upon circulatory ultrastructure and function. We hypothesized that microvascular pathologies occur in organs responsible for systemic Aβ peptide clearance in a model of AD and that Liraglutide (Victoza(®)) improves vessel architecture. METHODS: Seven-month-old APP/PS1 and age-matched wild-type mice received once-daily intraperitoneal injections of either Liraglutide or saline (n = 4 per group) for eight weeks. Casts of cerebral, splenic, hepatic, and renal microanatomy were analyzed using SEM. RESULTS: Casts from wild-type mice showed regularly spaced microvasculature with smooth lumenal…

medicine.medical_specialtyPhysiologySpleenMice TransgenicKidneyMicrocirculationAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseGlucagon-Like Peptide 1Physiology (medical)Internal medicinemedicinePresenilin-1AnimalsHumansHypoglycemic AgentsMolecular BiologyKidneybusiness.industryLiraglutideMicrocirculationBrainLiraglutideGlucagon-like peptide-1Extravasationmedicine.anatomical_structureEndocrinologyCerebrovascular CirculationCirculatory systemMicrovesselsSystemic administrationCardiology and Cardiovascular MedicinebusinessSpleenmedicine.drugMicrocirculation (New York, N.Y. : 1994)
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Prosurvival effect of human wild-type alpha-synuclein on MPTP-induced toxicity to central but not peripheral catecholaminergic neurons isolated from …

2010

In the present work we report the generation of a new line of alpha-synuclein (alpha-SYN) transgenic mice in which the human wild-type alpha-SYN cDNA is expressed under the control of a tyrosine hydroxylase (TH) promoter. We provide evidence that the ectopic protein is found in TH expressing neurons of both central and peripheral nervous systems. The transgene is expressed very early in development coinciding with the activity of the TH promoter and in the adult brain the human protein distributes normally to the nerve endings and cell bodies of dopaminergic nigral neurons without any evidence of abnormal aggregation. Our results indicate that expression of human wild-type alpha-SYN does no…

medicine.medical_specialtySympathetic Nervous SystemTyrosine 3-MonooxygenaseTransgeneMice Transgenicchemistry.chemical_compoundMiceCatecholaminesDopamineMesencephalonInternal medicinemedicineNeurotoxinAnimalsHumansTransgenesPromoter Regions GeneticCells CulturedDopamine transporterNeuronsDopamine Plasma Membrane Transport ProteinsTyrosine hydroxylasebiologyCell DeathGeneral NeuroscienceMPTPDopaminergicBrainEndocrinologynervous systemchemistry1-Methyl-4-phenyl-1236-tetrahydropyridineOrgan Specificitybiology.proteinalpha-SynucleinCatecholaminergic cell groupsmedicine.drugNeuroscience
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Aryl hydrocarbon receptor-dependent cell cycle arrest in isolated mouse oval cells

2013

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor, which mediates toxic responses to environmental pollutants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds. Besides its well known role in induction of xenobiotic metabolizing enzymes, for instance CYP1A1, the AhR is also involved in tumor promotion in rodents although the underlying mechanisms are still poorly understood. Additionally, the AhR is known to regulate cellular proliferation, which might result in either inhibition or stimulation of proliferation depending on the cell-type studied. Potential targets in hepatocarcinogenesis are liver oval (stem/progenitor) cells. In the pres…

medicine.medical_specialtyTCDDPolychlorinated DibenzodioxinsCell cycle checkpointBlotting WesternCyclin AMice TransgenicCyclin ATransfectionToxicologyRetinoblastoma ProteinCell LineMiceCyclin D1Proliferating Cell Nuclear AntigenInternal medicinemedicineAnimalsCyclin D1RNA Small InterferingTranscription factorCell Proliferationbiologyaryl hydrocarbon receptorRetinoblastoma proteinmouse oval cellsCell Cycle CheckpointsGeneral MedicineCell cycleAryl hydrocarbon receptorCell biologyEndocrinologyLiverReceptors Aryl Hydrocarbonbiology.proteinEnvironmental PollutantsTumor promotioncell cycle
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A common mechanism of action of the selective serotonin reuptake inhibitors citalopram and fluoxetine: Reversal of chronic psychosocial stress-induce…

2010

The transcription factor CREB regulates adaptive responses like memory consolidation, addiction, and synaptic refinement. Recently, chronic psychosocial stress as animal model of depression has been shown to stimulate CREB transcriptional activity in the brain; this stimulation was prevented by treatment with the antidepressant imipramine, which inhibits both noradrenaline and serotonin reuptake. However, it was unknown whether the selective inhibition of serotonin reuptake is sufficient for inhibition of stress-induced CREB activation, as it is for the clinical antidepressant effect. Therefore, the effect of two selective serotonin reuptake inhibitors (SSRIs), citalopram and fluoxetine, wa…

medicine.medical_specialtyTranscription GeneticMice TransgenicCitalopramBiologyCitalopramCREBImipramineDrug Administration ScheduleMice03 medical and health sciences0302 clinical medicineGenes ReporterCREB in cognitionFluoxetineInternal medicinemedicineAnimalsPhosphorylationCyclic AMP Response Element-Binding ProteinTranscription factor030304 developmental biologyPharmacology0303 health sciencesFluoxetineBrain3. Good healthEndocrinologyGene Expression RegulationMechanism of actionbiology.proteinAntidepressantmedicine.symptomSelective Serotonin Reuptake InhibitorsStress Psychological030217 neurology & neurosurgerymedicine.drugEuropean Journal of Pharmacology
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Sox17 regulates liver lipid metabolism and adaptation to fasting.

2014

Liver is a major regulator of lipid metabolism and adaptation to fasting, a process involving PPARalpha activation. We recently showed that the Vnn1 gene is a PPARalpha target gene in liver and that release of the Vanin-1 pantetheinase in serum is a biomarker of PPARalpha activation. Here we set up a screen to identify new regulators of adaptation to fasting using the serum Vanin-1 as a marker of PPARalpha activation. Mutagenized mice were screened for low serum Vanin-1 expression. Functional interactions with PPARalpha were investigated by combining transcriptomic, biochemical and metabolic approaches. We characterized a new mutant mouse in which hepatic and serum expression of Vanin-1 is …

medicine.medical_specialtyTransgeneMutantPeroxisome proliferator-activated receptorlcsh:MedicineMice TransgenicGastroenterology and HepatologyBiologyGPI-Linked ProteinsAmidohydrolasesMiceInternal medicineHMGB ProteinsMolecular Cell BiologymedicineMedicine and Health SciencesSOXF Transcription FactorsAnimalsPPAR alphalcsh:ScienceBeta oxidationchemistry.chemical_classificationMultidisciplinaryFatty liverlcsh:RBiology and Life SciencesLipid metabolismSOX9 Transcription FactorCell BiologyFastingmedicine.diseaseLipid MetabolismAdaptation Physiological3. Good healthEndocrinologychemistryPantetheinaseLiverlipids (amino acids peptides and proteins)lcsh:QTranscriptomeDrug metabolismResearch ArticlePLoS ONE
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP.

2008

Important targets for cAMP signalling in the heart are hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels that underlie the depolarizing 'pacemaker' current, I(f). We studied the role of I(f) in mice, in which binding of cAMP to HCN4 channels was abolished by a single amino-acid exchange (R669Q). Homozygous HCN4(R669Q/R669Q) mice die during embryonic development. Prior to E12, homozygous and heterozygous embryos display reduced heart rates and show no or attenuated responses to catecholaminergic stimulation. Adult heterozygous mice display normal heart rates at rest and during exercise. However, following beta-adrenergic stimulation, hearts exhibit pauses and sino-atrial…

medicine.medical_specialtymedicine.medical_treatmentCyclic Nucleotide-Gated Cation ChannelsEmbryonic DevelopmentStimulationMice TransgenicBiologyIn Vitro TechniquesGeneral Biochemistry Genetics and Molecular BiologyCardiac pacemakerArticleMiceHeart RatePregnancyInternal medicineHeart ratemedicineCyclic AMPHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsAnimalsMyocytes CardiacMolecular BiologyIon channelCells CulturedCatecholaminergicGeneral Immunology and MicrobiologyGeneral NeuroscienceEmbryogenesisDepolarizationEmbryoHeartMice Inbred C57BLEndocrinologyMutationFemaleThe EMBO journal
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Generating p53-specific cytotoxic T lymphocytes by recombinant adenoviral vector-based vaccination in mice, but not man.

2002

Mutations and aberrant expression of the p53 tumor suppressor protein are the most frequent molecular alterations in human malignancy. Peptides derived from the wild-type (wt) p53 protein and presented by major histocompatibility complex (MHC) molecules for T lymphocyte recognition are believed to serve as universal tumor-associated antigens for cancer immunotherapy. We studied the immunogeneicity of a recombinant replication-defective adenoviral vector encoding human full-length wt p53 (rAd/hup53) in human leukocyte antigen (HLA)-A2K(b)-transgenic (Tg) mice and man. The generation of p53 epitope-specific cytotoxic T lymphocytes (CTLs) in p53-proficient and p53-deficient A2K(b)-Tg mice was …

medicine.medical_treatmentGenetic VectorsEpitopes T-LymphocyteMice TransgenicPilot ProjectsHuman leukocyte antigenBiologyMajor histocompatibility complexCancer VaccinesEpitopeAdenoviridaeMiceImmune systemCancer immunotherapyAntigenSpecies SpecificityNeoplasmsHLA-A2 AntigenGeneticsmedicineCytotoxic T cellAnimalsHumansTreatment FailureMolecular BiologyT lymphocyteGenetic TherapyGenes p53Self ToleranceImmunologybiology.proteinMolecular MedicineTumor Suppressor Protein p53T-Lymphocytes CytotoxicGene therapy
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