Search results for " Inbred NOD"

showing 10 items of 76 documents

Cognate HLA absence in trans diminishes human NK cell education

2016

NK cells are innate lymphocytes with protective functions against viral infections and tumor formation. Human NK cells carry inhibitory killer cell Ig-like receptors (KIRs), which recognize distinct HLAs. NK cells with KIRs for self-HLA molecules acquire superior cytotoxicity against HLA– tumor cells during education for improved missing-self recognition. Here, we reconstituted mice with human hematopoietic cells from donors with homozygous KIR ligands or with a mix of hematopoietic cells from these homozygous donors, allowing assessment of the resulting KIR repertoire and NK cell education. We found that co-reconstitution with 2 KIR ligand–mismatched compartments did not alter the frequenc…

0301 basic medicine10028 Institute of Medical VirologyEpstein-Barr Virus InfectionsHerpesvirus 4 HumanCellchemical and pharmacologic phenomena610 Medicine & healthMice SCIDHuman leukocyte antigen2700 General MedicineAdaptive ImmunityBiology10263 Institute of Experimental Immunology03 medical and health sciencesMice Inbred NOD10049 Institute of Pathology and Molecular PathologymedicineAnimalsHumansCytotoxicityReceptorHistocompatibility Antigens Class IHEK 293 cellsGeneral MedicineAcquired immune systemKiller Cells NaturalHaematopoiesisHEK293 Cells030104 developmental biologymedicine.anatomical_structureNatural-Killer-Cells Cord Blood Transplantation Cytomegalovirus-Infection Class-I Inhibitory receptors Pediatric Patients TumorsImmunologyK562 CellsResearch ArticleK562 cells
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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Circulating exosomes deliver free fatty acids from the bloodstream to cardiac cells: Possible role of CD36

2019

Regulation of circulating free fatty acid (FFA) levels and delivery is crucial to maintain tissue homeostasis. Exosomes are nanomembranous vesicles that are released from diverse cell types and mediate intercellular communication by delivering bioactive molecules. Here, we sought to investigate the uptake of FFAs by circulating exosomes, the delivery of FFA-loaded exosomes to cardiac cells and the possible role of the FFA transporter CD36 in these processes. Circulating exosomes were purified from the serum of healthy donors after an overnight fast (F) or 20 minutes after a high caloric breakfast (postprandial, PP). Western blotting, Immunogold Electron Microscopy and FACS analysis of circu…

0301 basic medicineCD36 AntigensMaleLuminescenceCD36Mice SCIDFatty Acids NonesterifiedExosomesBiochemistryFatsMiceSpectrum Analysis TechniquesAnimal CellsMice Inbred NODMedicine and Health SciencesMyocytes CardiacTissue homeostasischemistry.chemical_classificationCardiomyocytesMultidisciplinarybiologymedicine.diagnostic_testPhysicsElectromagnetic RadiationQFatty AcidsRHeartFlow CytometryLipidsCell biologyBlotSpectrophotometryPhysical SciencesMedicinelipids (amino acids peptides and proteins)FemaleCytophotometryCellular Structures and OrganellesAnatomyCellular TypesResearch ArticleAdultScienceMuscle TissueResearch and Analysis MethodsFluorescenceFlow cytometryCell Line03 medical and health sciencesIn vivomedicineDiabetes MellitusAnimalsHumansVesiclesObesityRats WistarMuscle Cells030102 biochemistry & molecular biologyFatty acidBiology and Life SciencesCell BiologyAtherosclerosisMicrovesiclesDisease Models Animal030104 developmental biologyBiological Tissuechemistrybiology.proteinCardiovascular AnatomyEx vivoPLoS ONE
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The NSL Chromatin-Modifying Complex Subunit KANSL2 Regulates Cancer Stem-like Properties in Glioblastoma That Contribute to Tumorigenesis.

2016

KANSL2 is an integral subunit of the nonspecific lethal (NSL) chromatin-modifying complex that contributes to epigenetic programs in embryonic stem cells. In this study, we report a role for KANSL2 in regulation of stemness in glioblastoma (GBM), which is characterized by heterogeneous tumor stem-like cells associated with therapy resistance and disease relapse. KANSL2 expression is upregulated in cancer cells, mainly at perivascular regions of tumors. RNAi-mediated silencing of KANSL2 in GBM cells impairs their tumorigenic capacity in mouse xenograft models. In clinical specimens, we found that expression levels of KANSL2 correlate with stemness markers in GBM stem-like cell populations. M…

0301 basic medicineCHROMATINMaleCancer ResearchCarcinogenesisCellCell SeparationMice SCIDmedicine.disease_causeMiceCANCER STEM CELLMice Inbred NODHistone AcetyltransferasesOligonucleotide Array Sequence AnalysisBrain NeoplasmsNuclear ProteinsMiddle AgedFlow CytometryImmunohistochemistryChromatinUp-Regulationmedicine.anatomical_structureOncologyGene Knockdown TechniquesNeoplastic Stem CellsHeterograftsFemaleCIENCIAS NATURALES Y EXACTASAdultKANSLOtras Ciencias BiológicasBlotting WesternGLIOBLASTOMABiologyReal-Time Polymerase Chain ReactionArticleCiencias Biológicas03 medical and health sciencesCancer stem cellmedicineBiomarkers TumorGene silencingAnimalsHumansEpigeneticsAgedEmbryonic stem cell030104 developmental biologyCancer cellImmunologyCancer researchCarcinogenesisGlioblastomaCancer research
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MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

2018

AbstractMir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific lo…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal Transitionmedicine.medical_treatmentAntagomirSettore MED/50 - Scienze Tecniche Mediche ApplicateImmunologyTransplantation HeterologousOligonucleotidesBreast NeoplasmsBiologyArticleTargeted therapy03 medical and health sciencesCellular and Molecular NeuroscienceMiceBreast cancerErbBCell MovementMice Inbred NODOligonucleotideCell Line TumormicroRNAmedicineGene silencingAnimalsHumansEpithelial–mesenchymal transitionlcsh:QH573-671Neoplasm MetastasisCell ProliferationAnimallcsh:CytologyCancerAntagomirsMicroRNACell Biologymedicine.diseaseNeoplasm MetastasiMicroRNAs030104 developmental biologyCancer researchFemaleStem cellBreast NeoplasmHumanCell deathdisease
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Targeting the MET oncogene by concomitant inhibition of receptor and ligand via an antibody-"decoy" strategy

2018

MET, a master gene sustaining "invasive growth," is a relevant target for cancer precision therapy. In the vast majority of tumors, wild-type MET behaves as a "stress-response" gene and relies on the ligand (HGF) to sustain cell "scattering," invasive growth and apoptosis protection (oncogene "expedience"). In this context, concomitant targeting of MET and HGF could be crucial to reach effective inhibition. To test this hypothesis, we combined an anti-MET antibody (MvDN30) inducing "shedding" (i.e., removal of MET from the cell surface), with a "decoy" (i.e., the soluble extracellular domain of the MET receptor) endowed with HGF-sequestering ability. To avoid antibody/decoy interaction-and …

0301 basic medicineCancer ResearchLung NeoplasmsCellContext (language use)ApoptosisMice SCIDLigands03 medical and health sciencesMice0302 clinical medicineMice Inbred NODanti-HGF therapy; antibodies; decoy; MET oncogene; MET target therapyMET oncogeneExtracellularmedicineTumor Cells CulturedantibodiesAnimalsHumansdecoyCell ProliferationOncogenebiologyMET target therapyChemistryAntibodies MonoclonalProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysIn vitro030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellColonic NeoplasmsCancer researchbiology.proteinanti-HGF therapyFemaleAntibodyDecoyGlioblastoma
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Dual Constant Domain-Fab: A novel strategy to improve half-life and potency of a Met therapeutic antibody

2016

The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable…

0301 basic medicineCancer ResearchMice SCIDCancer targeted therapy0302 clinical medicineMice Inbred NODEpidermal growth factor receptorPhosphorylationbiologyChemistryImmunoglobulin Fab FragmentsAntibodies MonoclonalGeneral MedicineArticlesProto-Oncogene Proteins c-metHalf-lifeCell biologyOncology030220 oncology & carcinogenesisColonic NeoplasmsMetMolecular MedicineFemalemedicine.symptomSignal transductionAntibodySignal Transductionmedicine.drug_classColonAntibody; Cancer targeted therapy; Fab; Half-life; Met; Protein engineering; Cancer Research; Genetics; Molecular MedicineAntineoplastic AgentsMonoclonal antibody03 medical and health sciencesImmunoglobulin Fab FragmentsProtein DomainsCell Line TumormedicineGeneticsAnimalsHumansFabAntibodyCell growthMolecular biology030104 developmental biologyHEK293 CellsMechanism of actionHepatocyte Growth Factor ReceptorA549 Cellsbiology.proteinProtein engineering
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c-Fos induces chondrogenic tumor formation in immortalized human mesenchymal progenitor cells

2018

Mesenchymal progenitor cells (MPCs) have been hypothesized as cells of origin for sarcomas, and c-Fos transcription factor has been showed to act as an oncogene in bone tumors. In this study, we show c-Fos is present in most sarcomas with chondral phenotype, while multiple other genes are related to c-Fos expression pattern. To further define the role of c-Fos in sarcomagenesis, we expressed it in primary human MPCs (hMPCs), immortalized hMPCs and transformed murine MPCs (mMPCs). In immortalized hMPCs, c-Fos expression generated morphological changes, reduced mobility capacity and impaired adipogenic- and osteogenic-differentiation potentials. Remarkably, immortalized hMPCs or mMPCs express…

0301 basic medicineCarcinogenesisCelllcsh:MedicineMice SCIDArticleCell Line03 medical and health sciencesMice0302 clinical medicineMice Inbred NODmedicineAnimalsHumansProgenitor celllcsh:ScienceRegulation of gene expressionMultidisciplinaryOncogeneChemistryMesenchymal stem celllcsh:RGenes fosMesenchymal Stem CellsSarcomaChondrogenesisPhenotypeCell biologyGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticCell culture030220 oncology & carcinogenesislcsh:QProto-Oncogene Proteins c-fos
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Electrospun poly(hydroxybutyrate) scaffolds promote engraftment of human skin equivalents via macrophage M2 polarization and angiogenesis.

2018

Human dermo-epidermal skin equivalents (DE) comprising in vitro expanded autologous keratinocytes and fibroblasts are a good option for massive burn treatment. However, the lengthy expansion time required to obtain sufficient surface to cover an extensive burn together with the challenging surgical procedure limits their clinical use. The integration of DE and biodegradable scaffolds has been proposed in an effort to enhance their mechanical properties. Here, it is shown that poly(hydroxybutyrate) electrospun scaffolds (PHB) present good biocompatibility both in vitro and in vivo and are superior to poly-epsilon-caprolactone electrospun scaffolds as a substrate for skin reconstruction. Impl…

0301 basic medicineKeratinocytesMaleBiocompatibilityAngiogenesisPolymersBiomedical EngineeringMedicine (miscellaneous)HydroxybutyratesNeovascularization PhysiologicHuman skinhuman skin xenograftBiocompatible Materials02 engineering and technologyNodMice SCIDpoly(hydroxybutyrate)Biomaterials03 medical and health sciencesIn vivoMice Inbred NODProhibitinsHuman Umbilical Vein Endothelial CellsAnimalsHumansRats WistarelectrospinningCell ProliferationSkin ArtificialTissue EngineeringTissue ScaffoldsChemistryMacrophagestechnology industry and agricultureCell PolarityCell DifferentiationM2 polarizationDermisSkin Transplantation021001 nanoscience & nanotechnologyM2 MacrophageIn vitro030104 developmental biologyskin equivalentsEpidermis0210 nano-technologyBiomedical engineeringJournal of tissue engineering and regenerative medicine
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The cyto-protective effects of LH on ovarian reserve and female fertility during exposure to gonadotoxic alkylating agents in an adult mouse model.

2021

Abstract STUDY QUESTION Does LH protect mouse oocytes and female fertility from alkylating chemotherapy? SUMMARY ANSWER LH treatment before and during chemotherapy prevents detrimental effects on follicles and reproductive lifespan. WHAT IS KNOWN ALREADY Chemotherapies can damage the ovary, resulting in premature ovarian failure and reduced fertility in cancer survivors. LH was recently suggested to protect prepubertal mouse follicles from chemotoxic effects of cisplatin treatment. STUDY DESIGN, SIZE, DURATION This experimental study investigated LH effects on primordial follicles exposed to chemotherapy. Seven-week-old CD-1 female mice were randomly allocated to four experimental groups: C…

0301 basic medicineLHAlkylating Agentsfertility preservationmedia_common.quotation_subjectDNA repair LH cancer chemotherapy fertility preservation follicle protection ovoprotectionDNA repairOvaryMice SCIDBiologychemotherapyAndrology03 medical and health sciencesMice0302 clinical medicineOvarian FollicleMice Inbred NODPregnancyFollicular phasemedicineAnimalsHumanscancerFertility preservationOvarian follicleOvarian reserveOvarian ReserveOvulationmedia_commonReproductive Biology030219 obstetrics & reproductive medicineRehabilitationObstetrics and GynecologyOriginal ArticlesOocytemedicine.diseaseAcademicSubjects/MED00905Premature ovarian failure030104 developmental biologymedicine.anatomical_structureReproductive Medicinefollicle protectionovoprotectionlipids (amino acids peptides and proteins)FemaleHuman reproduction (Oxford, England)
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