Search results for "Growth factor"

showing 10 items of 1300 documents

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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A Transgenic Mouse Model of Inducible Macrophage Depletion

2009

Whether the wound macrophage is a key regulatory inflammatory cell type in skin repair has been a matter of debate. A transgenic mouse model mediating inducible macrophage depletion during skin repair has not been used to date to address this question. Here, we specifically rendered the monocyte/macrophage leukocyte lineage sensitive to diphtheria toxin by expressing the lysozyme M promoter-driven, Cre-mediated excision of a transcriptional STOP cassette from the simian DT receptor gene in mice (lysM-Cre/DTR). Application of diphtheria toxin to lysM-Cre/DTR mice led to a rapid reduction in both skin tissue and wound macrophage numbers at sites of injury. Macrophage-depleted mice revealed a …

Genetically modified mouseDiphtheria toxinSkin repairintegumentary systemMonocyteInflammationTransforming growth factor betaBiologyMolecular biologyPathology and Forensic MedicineCell biologymedicine.anatomical_structuremedicinebiology.proteinmedicine.symptomWound healingMyofibroblastThe American Journal of Pathology
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TGF-beta1 in liver fibrosis: an inducible transgenic mouse model to study liver fibrogenesis.

1999

Transforming growth factor-beta1 (TGF-beta1) is a powerful stimulus for collagen formation in vitro. To determine the in vivo effects of TGF-beta1 on liver fibrogenesis, we generated transgenic mice overexpressing a fusion gene [C-reactive protein (CRP)/TGF-beta1] consisting of the cDNA coding for an activated form of TGF-beta1 under the control of the regulatory elements of the inducible human CRP gene promoter. Two transgenic lines were generated with liver-specific overexpression of mature TGF-beta1. After induction of the acute phase response (15 h) with lipopolysaccharide (100 microgram ip), plasma TGF-beta1 levels reached600 ng/ml in transgenic animals, which is100 times above normal …

Genetically modified mouseLipopolysaccharidesmedicine.medical_specialtyTranscription GeneticPhysiologyTransgeneRecombinant Fusion ProteinsMice TransgenicBiologyRegulatory Sequences Nucleic AcidLiver Cirrhosis ExperimentalMiceDownregulation and upregulationFibrosisIn vivoTransforming Growth Factor betaPhysiology (medical)Internal medicinemedicineAnimalsHumansRNA MessengerPromoter Regions GeneticRegulation of gene expressionHepatologyGastroenterologymedicine.diseaseMolecular biologyImmunohistochemistryEndocrinologymedicine.anatomical_structureC-Reactive ProteinGene Expression RegulationLiverHepatocyteHepatic stellate cellCollagenProcollagen
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Spontaneous hepatic fibrosis in transgenic mice overexpressing PDGF-A.

2008

Platelet derived growth factor (PDGF) plays a central role in repair mechanisms after acute and chronic tissue damage. To further evaluate the role of PDGF-A in liver fibrogenesis in vivo, we generated transgenic mice with hepatocyte-specific overexpression of PDGF-A using the CRP-gene promoter. Transgenic but not wildtype mice showed expression of PDGF-A mRNA in the liver. Hepatic PDGF-A overexpression was accompanied by a significant increase in hepatic procollagen III mRNA expression as well as TGF-beta1 expression. Liver histology showed increased deposition of extracellular matrix in transgenic but not in wildtype mice. PDGF-A-transgenic mice showed positive sinusoidal staining for alp…

Genetically modified mouseLiver CirrhosisPlatelet-derived growth factorTransgeneGene ExpressionMice TransgenicTransforming Growth Factor beta1chemistry.chemical_compoundMiceFibrosisGeneticsmedicineAnimalsHumansRNA MessengerPlatelet-Derived Growth FactorbiologyGeneral Medicinemedicine.diseaseMolecular biologyRecombinant ProteinsC-Reactive ProteinCollagen Type IIIchemistryLiverHepatic stellate cellbiology.proteinHepatic fibrosisTyrosine kinasePlatelet-derived growth factor receptorSignal TransductionGene
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Chemical skin carcinogenesis is prevented in mice by the induced expression of a TGF-β related transgene

1995

Skin papillomas and squamous cell carcinomas (SCCs) are induced in mice by tumor initiation with a carcinogen followed by tumor promotion with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). These usually arise from preneoplastic lesions characterized by epidermal proliferation and hyperplasia, dermal edema, and inflammation. To evaluate the role of polypeptide growth factors in chemically induced skin carcinogenesis, we used transgenic mice carrying the cDNA for a TGF-β related molecule, bone morphogenetic protein-4 (BMP-4), under the control of the regulatory elements of the cytokeratin IV* gene in a skin carcinogenesis protocol. Control non-transgenic littermates and BMP-4 …

Genetically modified mouseMethylnitronitrosoguanidinePathologymedicine.medical_specialtySkin NeoplasmsHealth Toxicology and MutagenesisTransgenemedicine.medical_treatmentMice TransgenicTumor initiationBiologyToxicologymedicine.disease_causeMiceTransforming Growth Factor betaGeneticsmedicineAnimalsGenetics (clinical)SkinPapillomaintegumentary systemEpidermis (botany)ProteinsHyperplasiamedicine.diseaseCytokineBromodeoxyuridineOncologyBone Morphogenetic ProteinsCarcinoma Squamous CellCancer researchTetradecanoylphorbol AcetateTumor promotionEpidermisCarcinogenesisCell DivisionTeratogenesis, Carcinogenesis, and Mutagenesis
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Increased Expression of β6-Integrin in Skin Leads to Spontaneous Development of Chronic Wounds

2004

Integrin alphavbeta6 is an epithelial cell-specific receptor that is not normally expressed by resting epithelium but its expression is induced during wound healing. The function of alphavbeta6-integrin in wound repair is not clear. In the present study, we showed that beta6-integrin expression was strongly up-regulated in the epidermis in human chronic wounds but not in different forms of skin fibrosis. To test whether increased beta6-integrin expression plays a role in abnormal wound healing we developed four homozygous transgenic mouse lines that constitutively expressed human beta6-integrin in the epithelium. The mice developed normally and did not show any histological abnormalities in…

Genetically modified mousePathologymedicine.medical_specialtyIntegrin beta ChainsMice TransgenicBiologyPolymerase Chain ReactionPathology and Forensic MedicineCicatrixMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaFibrosismedicineAnimalsHumansIn Situ HybridizationSkin030304 developmental biologyWound Healing0303 health sciencesintegumentary systemEpidermis (botany)Transforming growth factor betamedicine.diseaseFibrosisImmunohistochemistryEpithelium3. Good healthBlotting Southernmedicine.anatomical_structure030220 oncology & carcinogenesisChronic Diseasebiology.proteinImmunohistochemistryWound healingRegular ArticlesTransforming growth factorThe American Journal of Pathology
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TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

2004

Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-depende…

Genetically modified mouseSTAT3 Transcription FactorColorectal cancerRecombinant Fusion ProteinsT-LymphocytesImmunologyBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicProtein Serine-Threonine KinasesMiceIn vivoTransforming Growth Factor betamedicineImmunology and AllergyAnimalsHumansEndoscopy Digestive SystemIntestinal MucosaInterleukin 6Autocrine signallingMice KnockoutbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionReceptor Transforming Growth Factor-beta Type IIHistologymedicine.diseaseImmunohistochemistryReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalInfectious DiseasesTumor progressionImmunologyColonic NeoplasmsCancer researchbiology.proteinDisease ProgressionTrans-ActivatorsReceptors Transforming Growth Factor betaTransforming growth factorSignal TransductionImmunity
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A novel in vivo inducible dendritic cell ablation model in mice

2010

Abstract Dendritic cells (DCs) are involved in T cell activation via their uptake and presentation of antigens. In vivo function of DCs was analyzed using transgenic mouse models that express diphtheria toxin receptor (DTR) or the diphtheria toxin-A subunit (DTA) under the control of the CD11c/Itgax promoter. However, CD11c+ cells are heterogeneous populations that contain several DC subsets. Thus, the in vivo function of each subset of DCs remains to be elucidated. Here, we describe a new inducible DC ablation model, in which DTR expression is induced under the CD11c/Itgax promoter after Cre-mediated excision of a stop cassette (CD11c-iDTR). Crossing of CD11c-iDTR mice with CAG-Cre transge…

Genetically modified mouseT cellBiophysicsCD11cCre recombinaseMice Transgenicchemical and pharmacologic phenomenaBiologyBiochemistryMiceAntigenIn vivomedicineAnimalsPromoter Regions GeneticMolecular BiologyIntegraseshemic and immune systemsDendritic CellsCell BiologyDendritic cellMolecular biologyIn vitroCD11c Antigenmedicine.anatomical_structureModels AnimalIntercellular Signaling Peptides and ProteinsHeparin-binding EGF-like Growth FactorBiochemical and Biophysical Research Communications
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TGFbeta regulates the CD4+CD25+ T-cell pool and the expression of Foxp3 in vivo.

2004

Factors influencing the development of CD4+CD25+ T-cells in vivo are poorly understood. In order to investigate the contribution of TGFbeta1 to the development and function of CD4+CD25+ T-cells, we generated a gain of function mutation resulting in the overexpression of an active form of TGFbeta1 in T-cells under control of the human CD2 promoter. In peripheral lymphoid organs and in the thymus, the frequency of CD4+CD25+ T-cells was increased in transgenic mice. This appeared to be due to an autocrine effect of TGFbeta on T-cells, since concomitant impairment of TGFbeta-signaling in double transgenic mice resulted in a phenotype similar to wild type. In contrast, in single transgenic mice …

Genetically modified mouseTransgeneT cellImmunologyCD2 AntigensMice TransgenicBiologyMiceIn vivoT-Lymphocyte SubsetsTransforming Growth Factor betamedicineImmunology and AllergyAnimalsAutocrine signallingTranscription factorWild typeFOXP3Forkhead Transcription FactorsReceptors Interleukin-2General MedicineMolecular biologyCell biologyInterleukin-10DNA-Binding Proteinsmedicine.anatomical_structureCD4 AntigensInternational immunology
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