Search results for " 129 Strain"

showing 10 items of 13 documents

Thy-1 (CD90) regulates the extravasation of leukocytes during inflammation.

2010

Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung infl…

ChemokineMice 129 StrainNeutrophilsmedicine.medical_treatmentT-LymphocytesImmunologyInflammationCD18In Vitro TechniquesPeritonitisMonocytesMiceCell MovementCell AdhesionLeukocytesImmunology and AllergyMedicineAnimalsHumansCD90Thy-1InflammationMice KnockoutTransplantation Chimerabiologybusiness.industryInterleukinsEndothelial CellsPneumoniaExtravasationTransplantationEosinophilsMice Inbred C57BLCytokineIntegrin alpha MImmunologybiology.proteinThy-1 Antigensmedicine.symptomChemokinesbusinessextravasationPeptide HydrolasesEuropean journal of immunology
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Injury-activated glial cells promote wound healing of the adult skin in mice

2018

Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously…

0301 basic medicine10017 Institute of AnatomyGeneral Physics and AstronomyTransforming Growth Factor betaMedicinelcsh:ScienceMyofibroblastsCells CulturedSkinMice KnockoutMultidisciplinaryintegumentary systemSOXE Transcription FactorsQCell CycleCell Differentiation3100 General Physics and AstronomyCell biologyMice Inbred DBACutaneous woundMyofibroblastNeurogliaSignal TransductionMice 129 StrainScienceMice Transgenic610 Medicine & health1600 General ChemistryGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesParacrine signallingDownregulation and upregulationIn vivoFate mapping1300 General Biochemistry Genetics and Molecular BiologyAnimalsHumansEpithelial proliferationWound Healingbusiness.industryGene Expression ProfilingGeneral ChemistryMice Inbred C57BL030104 developmental biology10032 Clinic for Oncology and Hematology570 Life sciences; biologylcsh:QWound healingbusiness
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LRP1 mediates bidirectional transcytosis of amyloid-β across the blood-brain barrier.

2011

According to the "amyloid hypothesis", the amyloid-β (Aβ) peptide is the toxic intermediate driving Alzheimer's disease (AD) pathogenesis. Recent evidence suggests that the low density lipoprotein receptor-related protein 1 (LRP1) transcytoses Aβ out of the brain across the blood-brain barrier (BBB). To provide genetic evidence for LRP1-mediated transcytosis of Aβ across the BBB we analyzed Aβ transcytosis across primary mouse brain capillary endothelial cells (pMBCECs) derived from wild-type and LRP1 knock-in mice. Here, we show that pMBCECs in vitro express functionally active LRP1. Moreover, we demonstrate that LRP1 mediates transcytosis of [(125)I]-Aβ(1-40) across pMBCECs in both direct…

AgingMice 129 StrainEndogenyBiologyEndocytosisBlood–brain barrierchemistry.chemical_compoundMicemedicineAnimalsGene Knock-In TechniquesReceptorCells CulturedAmyloid beta-PeptidesGeneral NeuroscienceTumor Suppressor ProteinsMolecular biologyLRP1Peptide FragmentsBiochemistry of Alzheimer's diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryTranscytosisReceptors LDLBlood-Brain BarrierLow-density lipoproteinNeurology (clinical)Geriatrics and GerontologyTranscytosisLow Density Lipoprotein Receptor-Related Protein-1Developmental BiologyNeurobiology of aging
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RORC1 Regulates Tumor-Promoting "Emergency" Granulo-Monocytopoiesis

2015

Cancer-driven granulo-monocytopoiesis stimulates expansion of tumor promoting myeloid populations, mostly myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). We identified subsets of MDSCs and TAMs based on the expression of retinoic-acid-related orphan receptor (RORC1/RORγ) in human and mouse tumor bearers. RORC1 orchestrates myelopoiesis by suppressing negative (Socs3 and Bcl3) and promoting positive (C/EBPβ) regulators of granulopoiesis, as well as the key transcriptional mediators of myeloid progenitor commitment and differentiation to the monocytic/macrophage lineage (IRF8 and PU.1). RORC1 supported tumor-promoting innate immunity by protecting MDSCs from …

MaleCancer ResearchMyeloidNeutrophilsMacrophageCellular differentiationApoptosisMonocyteMonocyteshemic and lymphatic diseasesMyeloid CellsSOCS3Myeloid CellMyelopoiesisMice KnockoutMicroscopy ConfocalReverse Transcriptase Polymerase Chain ReactionMedicine (all)NeutrophilCell DifferentiationNuclear Receptor Subfamily 1 Group F Member 3Animals; Apoptosis; Cell Differentiation; Cell Line Tumor; Cytokines; Female; Gene Expression Regulation Neoplastic; Granulocytes; Humans; Immunohistochemistry; Macrophages; Male; Mice 129 Strain; Mice Inbred C57BL; Mice Knockout; Microscopy Confocal; Monocytes; Myeloid Cells; Myelopoiesis; Neoplasms Experimental; Neutrophils; Nuclear Receptor Subfamily 1 Group F Member 3; Reverse Transcriptase Polymerase Chain Reaction; Tumor Burden; Cancer Research; Cell Biology; Oncology; Medicine (all)ImmunohistochemistryTumor BurdenGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyCytokinesFemaleMyelopoiesisHumanMice 129 StrainBiologySettore MED/08 - Anatomia PatologicaGranulopoiesisArticleMyelopoiesiCell Line TumormedicineAnimalsHumansCytokineInnate immune systemAnimalMacrophagesApoptosiGranulocyteNeoplasms ExperimentalCell BiologyMice Inbred C57BLImmunologyCancer researchIRF8Granulocytes
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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G protein-coupled odorant receptors underlie mechanosensitivity in mammalian olfactory sensory neurons

2014

Mechanosensitive cells are essential for organisms to sense the external and internal environments, and a variety of molecules have been implicated as mechanical sensors. Here we report that odorant receptors (ORs), a large family of G protein-coupled receptors, underlie the responses to both chemical and mechanical stimuli in mouse olfactory sensory neurons (OSNs). Genetic ablation of key signaling proteins in odor transduction or disruption of OR–G protein coupling eliminates mechanical responses. Curiously, OSNs expressing different OR types display significantly different responses to mechanical stimuli. Genetic swap of putatively mechanosensitive ORs abolishes or reduces mechanical res…

Mice 129 StrainPatch-Clamp TechniquesG protein[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionSensory systemMice Transgenicodorant receptorsBiologyReceptors OdorantMechanotransduction CellularOlfactory Receptor NeuronsMiceg protein-coupled receptorsAnimalsHumansCalcium SignalingMechanotransductionReceptorG protein-coupled receptormechanotransductionMice KnockoutMultidisciplinaryheterologous expressionBiological SciencesRecombinant ProteinsMice Inbred C57BLHEK293 CellsMice Inbred DBA[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Mutagenesis Site-DirectedEctopic expressionMechanosensitive channels[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]NeuroscienceTransduction (physiology)Mechanoreceptors[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionmechanical sensorsSignal Transduction
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Murine cytomegalovirus (CMV) infection via the intranasal route offers a robust model of immunity upon mucosal CMV infection

2016

Cytomegalovirus (CMV) is a ubiquitous virus, causing the most common congenital infection in humans, yet a vaccine against this virus is not available. Experimental studies of immunity against CMV in animal models of infection, such as the infection of mice with mouse CMV (MCMV), have relied mainly on parenteral infection protocols, although the virus naturally transmits by mucosal routes via body fluids. To characterize the biology of infections by mucosal routes, we compared the kinetics of virus replication, latent viral load and CD8 T-cell responses in lymphoid organs upon experimental intranasal (targeting the respiratory tract) and intragastric (targeting the digestive tract) infectio…

0301 basic medicineMuromegalovirusMice 129 StrainCongenital cytomegalovirus infectionSpleenCD8-Positive T-LymphocytesBiologyVirus ReplicationVirus03 medical and health sciencesImmunityVirologyVirus latencymedicineAnimalsImmunity MucosalMice Inbred BALB CAnimal StructuresViral Loadmedicine.diseaseVirologyVirus Latency030104 developmental biologymedicine.anatomical_structureLymphatic systemViral replicationModels AnimalImmunologyFemaleViral load
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Innate Effector-Memory T-Cell Activation Regulates Post-Thrombotic Vein Wall Inflammation and Thrombus Resolution

2016

Rationale: Immune cells play an important role during the generation and resolution of thrombosis. T cells are powerful regulators of immune and nonimmune cell function, however, their role in sterile inflammation in venous thrombosis has not been systematically examined. Objective: This study investigated the recruitment, activation, and inflammatory activity of T cells in deep vein thrombosis and its consequences for venous thrombus resolution. Methods and Results: CD4 + and CD8 + T cells infiltrate the thrombus and vein wall rapidly on deep vein thrombosis induction and remain in the tissue throughout the thrombus resolution. In the vein wall, recruited T cells largely consist of effect…

CD4-Positive T-Lymphocytes0301 basic medicineChemokineMice 129 StrainPhysiologyMice TransgenicInflammationCD8-Positive T-Lymphocytes030204 cardiovascular system & hematologyVaricose VeinsMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansThrombusVeinInflammationVenous ThrombosisbiologyEffector Memory T-CellThrombosismedicine.diseaseThrombosisImmunity InnateCell biologyMice Inbred C57BLVenous thrombosis030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinmedicine.symptomCardiology and Cardiovascular MedicineCirculation Research
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Stabilization of Perivascular Mast Cells by Endothelial CNP (C-Type Natriuretic Peptide)

2020

Objective: Activated perivascular mast cells (MCs) participate in different cardiovascular diseases. Many factors provoking MC degranulation have been described, while physiological counterregulators are barely known. Endothelial CNP (C-type natriuretic peptide) participates in the maintenance of vascular barrier integrity, but the target cells and mechanisms are unclear. Here, we studied whether MCs are regulated by CNP. Approach and Results: In cultured human and murine MCs, CNP activated its specific GC (guanylyl cyclase)-B receptor and cyclic GMP signaling. This enhanced cyclic GMP–dependent phosphorylation of the cytoskeleton-associated VASP (vasodilator-stimulated phosphoprotein) and…

medicine.medical_specialtyMice 129 StrainMedizinMyocardial Reperfusion InjuryCell DegranulationCell LineMicrocirculationCapillary PermeabilityCyclic gmpAdenosine TriphosphateInternal medicineParacrine CommunicationmedicineAnimalsMast CellsPhosphorylationCyclic GMPMice KnockoutChemistryMicrofilament ProteinsDegranulationEndothelial CellsNatriuretic Peptide C-TypeThrombosisPhosphoproteinsMice Inbred C57BLDisease Models AnimalEndocrinologyNeutrophil InfiltrationC-type natriuretic peptideCardiology and Cardiovascular MedicineCell Adhesion MoleculesReceptors Atrial Natriuretic FactorSignal TransductionGuanylate cyclase
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Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
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