Search results for " Transgenic"

showing 10 items of 522 documents

No effect of C-reactive protein on early atherosclerosis in LDLR-/- / human C-reactive protein transgenic mice

2008

summaryThe association between increased concentrations of C-reactive protein (CRP) and future cardiovascular events is well established. However, it is currently unclear whether this clinical observation represents an epiphenomenon or whether the pentraxin may actively promote the development of atherosclerosis. Experimental studies with knockout mice with a defect in apolipoprotein E (ApoE-/-) have been used to investigate the role of CRP in atherogenesis, but the results obtained have been contradictory so far. Since knockout mice with a defect in low density lipoprotein receptor (LDLR-/-) may represent a better model of atherogenesis compared to ApoE-/- animals, we undertook experiments…

Genetically modified mouseApolipoprotein ETime FactorsGenotypeLipoproteinsTransgeneMice TransgenicBiologyLesionMicemedicineAnimalsHumansComplement ActivationAortaCrosses GeneticMice KnockoutC-reactive proteinAcute-phase proteinHematologyAtherosclerosisDietary FatsLipidsDisease Models AnimalC-Reactive ProteinPhenotypeReceptors LDLImmunologyLDL receptorKnockout mousebiology.proteinlipids (amino acids peptides and proteins)medicine.symptomThrombosis and Haemostasis
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Overexpression of TGF-ß1 in macrophages reduces and stabilizes atherosclerotic plaques in ApoE-deficient mice.

2011

Although macrophages represent the hallmark of both human and murine atherosclerotic lesions and have been shown to express TGF-ß1 (transforming growth factor β1) and its receptors, it has so far not been experimentally addressed whether the pleiotropic cytokine TGF-ß1 may influence atherogenesis by a macrophage specific mechanism. We developed transgenic mice with macrophage specific TGF-ß1 overexpression, crossed the transgenics to the atherosclerotic ApoE (apolipoprotein E) knock-out strain and quantitatively analyzed both atherosclerotic lesion development and composition of the resulting double mutants. Compared with control ApoE(-/-) mice, animals with macrophage specific TGF-ß1 overe…

Genetically modified mouseApolipoprotein Emedicine.medical_specialtyPathologyHistologyMouseSciencemedicine.medical_treatmentImmune CellsImmunologyAntigen-Presenting CellsMice TransgenicBiologyCardiovascularLesionTransforming Growth Factor beta1MiceApolipoproteins EModel OrganismsVascular BiologyInternal medicinemedicineGeneticsMacrophageAnimalsReceptorBiologyMice KnockoutMultidisciplinaryMacrophagesQRAnimal ModelsAtherosclerosisImmunohistochemistryPlaque AtheroscleroticCytokineEndocrinologyImmunohistochemistryMedicineFemalemedicine.symptomGene FunctionTransforming growth factorResearch ArticlePloS one
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Cholesterol and Amyloid-β: Evidence for a Cross-Talk between Astrocytes and Neuronal Cells.

2011

Accumulating data supports the concept that alterations of cholesterol metabolism might influence the development of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive accumulation of amyloid-β (Aβ) peptides in the brain. Changes in the neuronal production of Aβ have been described as a function of cholesterol levels, thus suggesting a causal link between cholesterol homeostasis dysregulation and AD pathogenesis. Under physiological conditions, cholesterol uptake in the brain is efficiently prevented by the blood-brain barrier, and mature neurons are thought to rely on glial cells for their cholesterol supply. In the present study, we tested the hypothesis t…

Genetically modified mouseBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicCell LinePathogenesisMicechemistry.chemical_compoundAlzheimer DiseasemedicineAnimalsHomeostasisHumansBrain ChemistryNeuronsAmyloid beta-PeptidesbiologyCholesterolGeneral NeuroscienceTransporterReceptor Cross-TalkGeneral Medicinemedicine.diseaseCoculture TechniquesPsychiatry and Mental healthClinical PsychologyCholesterolATP Binding Cassette Transporter 1chemistryAstrocytesABCA1biology.proteinATP-Binding Cassette Transporterslipids (amino acids peptides and proteins)Geriatrics and GerontologyAlzheimer's diseaseNeuroscienceHomeostasisATP Binding Cassette Transporter 1
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Liver-specific overexpression of matrix metalloproteinase 9 (MMP-9) in transgenic mice accelerates development of hepatocellular carcinoma.

2010

Matrix metalloproteinase-9 (MMP-9) plays a central role in tumor invasion and development of metastases. Expression of MMP-9 had been shown in human hepatocellular carcinomas (HCCs). However, it remained unclear whether MMP-9 could influence development of HCC. In order to address this issue, we generated transgenic mice overexpressing MMP-9 in the liver. In order to avoid embryonic lethality a Cre-lox system was utilized for conditional overexpression of MMP-9 under control of an albumin enhancer and promoter. Induction of MMP-9 overexpression in transgenic mice was achieved by i.v. injection of an adenovirus coding for the Cre recombinase. Initiation of liver carcinogenesis was achieved b…

Genetically modified mouseCancer ResearchLiver tumorTransgeneGenetic VectorsCre recombinaseGene ExpressionMice TransgenicBiologymedicine.disease_causeMiceLiver Neoplasms ExperimentalIn vivoGene OrdermedicineAnimalsHomeostasisHumansHomologous RecombinationMolecular BiologyIntegrasesHCCSmedicine.diseaseMolecular biologyCell Transformation NeoplasticPhenotypeLiverMatrix Metalloproteinase 9Organ SpecificityHepatocellular carcinomaCarcinogenesisMolecular carcinogenesis
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Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function

2001

Up-regulation of proapoptotic genes has been reported in heart failure and myocardial infarction. To determine whether caspase genes can affect cardiac function, a transgenic mouse was generated. Cardiac tissue-specific overexpression of the proapoptotic gene Caspase3 was induced by using the rat promoter of α-myosin heavy chain, a model that may represent a unique tool for investigating new molecules and antiapoptotic therapeutic strategies. Cardiac-specific Caspase3 expression induced transient depression of cardiac function and abnormal nuclear and myofibrillar ultrastructural damage. When subjected to myocardial ischemia–reperfusion injury, Caspase3 transgenic mice showed increased inf…

Genetically modified mouseCardiac function curveDNA ComplementaryTransgeneRecombinant Fusion ProteinsMyocardial InfarctionMyocardial IschemiaCaspase 3ApoptosisMice TransgenicMyocardial Reperfusion InjuryDNA FragmentationContractilityMiceVentricular Dysfunction LeftmedicineAnimalsHumansGenetic Predisposition to DiseaseMyocardial infarctionCaspaseMultidisciplinarybiologyCaspase 3MyocardiumBiological Sciencesmedicine.diseasePhenotypeGene Expression RegulationEchocardiographyOrgan SpecificityHeart failureCaspasesCancer researchbiology.proteincardiovascular system
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A Cre-inducible diphtheria toxin receptor mediates cell lineage ablation after toxin administration.

2004

A new system for lineage ablation is based on transgenic expression of a diphtheria toxin receptor (DTR) in mouse cells and application of diphtheria toxin (DT). To streamline this approach, we generated Cre-inducible DTR transgenic mice (iDTR) in which Cre-mediated excision of a STOP cassette renders cells sensitive to DT. We tested the iDTR strain by crossing to the T cell- and B cell-specific CD4-Cre and CD19-Cre strains, respectively, and observed efficient ablation of T and B cells after exposure to DT. In MOGi-Cre/iDTR double transgenic mice expressing Cre recombinase in oligodendrocytes, we observed myelin loss after intraperitoneal DT injections. Thus, DT crosses the blood-brain bar…

Genetically modified mouseCell SurvivalTransgeneT cellT-LymphocytesCellCre recombinaseApoptosisMice TransgenicReceptors Cell SurfaceBiologyBiochemistryCell LineMicemedicineAnimalsCell LineageDiphtheria ToxinReceptorMolecular BiologyDiphtheria toxinIntegrasesCell DifferentiationCell BiologyMolecular biologyRecombinant ProteinsOligodendrogliamedicine.anatomical_structureCell cultureIntercellular Signaling Peptides and ProteinsBiotechnologyHeparin-binding EGF-like Growth FactorNature methods
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Impairment of TGF-β signaling in T cells increases susceptibility to experimental autoimmune hepatitis in mice

2002

In autoimmune hepatitis, strong TGF-beta1 expression is found in the inflamed liver. TGF-beta overexpression may be part of a regulatory immune response attempting to suppress autoreactive T cells. To test this hypothesis, we determined whether impairment of TGF-beta signaling in T cells leads to increased susceptibility to experimental autoimmune hepatitis (EAH). Transgenic mice of strain FVB/N were generated expressing a dominant-negative TGF-beta type II receptor in T cells under the control of the human CD2 promoter/locus control region. On induction of EAH, transgenic mice showed markedly increased portal and periportal leukocytic infiltrations with hepatocellular necroses compared wit…

Genetically modified mouseCellular immunityPhysiologyT-LymphocytesEnzyme-Linked Immunosorbent AssayMice TransgenicAutoimmune hepatitisBiologyMiceImmune systemTransforming Growth Factor betaPhysiology (medical)medicineAnimalsHomeostasisCells CulturedAutoimmune diseaseHepatitisB-LymphocytesHepatologyGastroenterologyT lymphocyteBlotting Northernmedicine.diseaseImmunohistochemistryHepatitis AutoimmunePhenotypeNeutrophil InfiltrationImmunologySignal transductionSignal TransductionAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Astrocytic alterations in interleukin-6/Soluble interleukin-6 receptor alpha double-transgenic mice.

2000

Interleukin-6 (IL-6), a major cytokine with diverse effects on cells mainly of the immune and hematopoietic systems, has been linked to several neurological disorders such as acquired immune deficiency syndrome dementia, multiple sclerosis, and Alzheimer's disease. Central nervous system (CNS)-specific expression of IL-6 caused neurodegeneration, massive gliosis, and vascular proliferation in transgenic mice. However, the effects of systemically circulating IL-6 and its receptor IL-6Ralpha on the CNS are unknown. IL-6Ralpha is the specific component of the IL-6 receptor system and hence an important co-factor of IL-6. IL-6Ralpha is bioactive in a membrane-bound and in a soluble (s) form. We…

Genetically modified mouseCentral Nervous SystemPathologymedicine.medical_specialtyTransgeneCentral nervous systemGene ExpressionMice TransgenicBiologyPathology and Forensic MedicineMicemedicineAnimalsHumansTransgenesReceptorInterleukin 6Interleukin-6NeurodegenerationBrainmedicine.diseaseReceptors Interleukin-6Astrogliosismedicine.anatomical_structurePhenotypeGliosisSolubilityAstrocytesbiology.proteinmedicine.symptomRegular ArticlesThe American journal of pathology
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Profilin1 activity in cerebellar granule neurons is required for radial migration in vivo.

2014

Neuron migration defects are an important aspect of human neuropathies. The underlying molecular mechanisms of such migration defects are largely unknown. Actin dynamics has been recognized as an important determinant of neuronal migration, and we recently found that the actin-binding protein profilin1 is relevant for radial migration of cerebellar granule neurons (CGN). As the exploited brain-specific mutants lacked profilin1 in both neurons and glial cells, it remained unknown whether profilin1 activity in CGN is relevant for CGN migration in vivo. To test this, we capitalized on a transgenic mouse line that expresses a tamoxifen-inducible Cre variant in CGN, but no other cerebellar cell …

Genetically modified mouseCerebellumNeurogenesisShort CommunicationMutantMice TransgenicBiologyCellular and Molecular NeuroscienceMiceProfilinsIn vivoCell MovementCerebellummedicineAnimalsActin-binding proteinNeuronsCell BiologyActinsCell biologyTreadmillingmedicine.anatomical_structureProfilinCerebellar cortexbiology.proteinNeurogliaCell adhesionmigration
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Inhibition of the HER2 pathway by n-3 polyunsaturated fatty acids prevents breast cancer in fat-1 transgenic mice

2013

Overexpression of the tyrosine kinase receptor, ErbB2/HER2/Neu, occurs in 25–30% of invasive breast cancer (BC) with poor patient prognosis. Due to confounding factors, inconsistencies still remain regarding the protective effects of n-3 polyunsaturated fatty acids (PUFAs) on BC. We therefore evaluated whether fat-1 transgenic mice, endogenously synthesizing n-3 PUFAs from n-6 PUFAs, were protected against BC development, and we then aimed to study in vivo a mechanism potentially involved in such protection. E0771 BC cells were implanted into fat-1 and wild-type (WT) mice. After tumorigenesis examination, we analyzed the expression of proteins involved in the HER2 signaling pathway and lipi…

Genetically modified mouseFatty Acid DesaturasesDocosahexaenoic AcidsReceptor ErbB-3Receptor ErbB-2Breast NeoplasmsMice TransgenicQD415-436Biologymedicine.disease_causexenograft preventionBiochemistryReceptor tyrosine kinaseProto-Oncogene Proteins c-mycMiceEndocrinologyDownregulation and upregulationCell Line TumorFatty Acids Omega-3medicineAnimalsHumansCaenorhabditis elegans ProteinsResearch ArticlesCell Proliferationchemistry.chemical_classificationCell growthCell BiologyXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticMice Inbred C57BLchemistryDocosahexaenoic acidImmunologyn-3 tissue enrichmentbiology.proteinCancer researchFemaleSignal transductionCarcinogenesispolyunsaturated fatty acid-derived mediatorsPolyunsaturated fatty acidSignal TransductionJournal of Lipid Research
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