Search results for "Loi"

showing 10 items of 4617 documents

Targeting distinct myeloid cell populations in vivo using polymers, liposomes and microbubbles

2016

Identifying intended or accidental cellular targets for drug delivery systems is highly relevant for evaluating therapeutic and toxic effects. However, limited knowledge exists on the distribution of nano- and micrometer-sized carrier systems at the cellular level in different organs. We hypothesized that clinically relevant carrier materials, differing in composition and size, are able to target distinct myeloid cell subsets that control inflammatory processes, such as macrophages, neutrophils, monocytes and dendritic cells. Therefore, we analyzed the biodistribution and in vivo cellular uptake of intravenously injected poly(N-(2-hydroxypropyl) methacrylamide) polymers, PEGylated liposomes…

0301 basic medicineBiodistributionMyeloidPolymersCellBiophysicsMice NudeCapsulesBioengineeringSpleen02 engineering and technologyFlow cytometryBiomaterialsMice03 medical and health sciencesNanocapsulesIn vivoMaterials TestingmedicineAnimalsMyeloid CellsTissue DistributionMolecular Targeted TherapyMicrobubblesmedicine.diagnostic_testbusiness.industryMacrophages021001 nanoscience & nanotechnology3. Good healthCell biologyVisceraNanomedicine030104 developmental biologymedicine.anatomical_structureOrgan SpecificityMechanics of Materials2023 OA procedureLiposomesImmunologyDrug deliveryCeramics and CompositesMicrobubblesTargeted delivery0210 nano-technologybusinessBiomaterials
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Adhesion G protein-coupled receptor VLGR1/ADGRV1 regulates cell spreading and migration by mechanosensing at focal adhesions.

2021

Summary VLGR1 (very large G protein-coupled receptor-1) is by far the largest adhesion G protein-coupled receptor in humans. Homozygous pathologic variants of VLGR1 cause hereditary deaf blindness in Usher syndrome 2C and haploinsufficiency of VLGR1 is associated with epilepsy. However, its molecular function remains elusive. Herein, we used affinity proteomics to identify many components of focal adhesions (FAs) in the VLGR1 interactome. VLGR1 is localized in FAs and assembles in FA protein complexes in situ. Depletion or loss of VLGR1 decreases the number and length of FAs in hTERT-RPE1 cells and in astrocytes of Vlgr1 mutant mice. VLGR1 depletion reduces cell spread and migration kinetic…

0301 basic medicineBiomoleculesMultidisciplinaryChemistryScienceQCell02 engineering and technologyCell Biology021001 nanoscience & nanotechnologyProteomicsInteractomeArticleCell biologyFocal adhesion03 medical and health sciences030104 developmental biologyMetabotropic receptormedicine.anatomical_structuremedicine0210 nano-technologyHaploinsufficiencyReceptorMolecular BiologyG protein-coupled receptoriScience
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Haploinsufficiency of the Primary Familial Brain Calcification Gene SLC20A2 Mediated by Disruption of a Regulatory Element

2020

OBJECTIVE Primary familial brain calcification (PFBC) is a rare cerebral microvascular calcifying disorder with diverse neuropsychiatric expression. Five genes were reported as PFBC causative when carrying pathogenic variants. Haploinsufficiency of SLC20A2, which encodes an inorganic phosphate importer, is a major cause of autosomal-dominant PFBC. However, PFBC remains genetically unexplained in a proportion of patients, suggesting the existence of additional genes or cryptic mutations. We analyzed exome sequencing data of 71 unrelated, genetically unexplained PFBC patients with the aim to detect copy number variations that may disrupt the expression of core PFBC-causing genes. METHODS Afte…

0301 basic medicineBrain DiseasesDNA Copy Number VariationsSodium-Phosphate Cotransporter Proteins Type IIIHEK 293 cellsBrainHaploinsufficiencyBiologyMolecular biologyReverse transcriptase03 medical and health sciencesHEK293 Cells030104 developmental biology0302 clinical medicineNeurologyMutationHumansNeurology (clinical)Copy-number variationAlleleHaploinsufficiencyEnhancerGene030217 neurology & neurosurgeryExome sequencingMovement Disorders
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HLA-DPB1 mismatch alleles represent powerful leukemia rejection antigens in CD4 T-cell immunotherapy after allogeneic stem-cell transplantation.

2016

Refractory or relapsed acute myeloid leukemia (AML) represents a frequent complication after allogeneic hematopoietic stem-cell transplantation (HSCT). We show herein that primary in vitro stimulation of CD45RA-selected CD4 T cells of stem-cell donors with 10/10 HLA-matched AML blasts results in expansion of cytolytic T-lymphocytes (CTL) that almost all recognize HLA-DPB1 mismatch alleles, which clinically occur in up to 80% of donor-patient pairs. Primary AML blasts were found to strongly express HLA-DPB1, whereas fibroblasts and keratinocytes used as surrogate target cells for graft-versus-host disease did express HLA-DPB1 only upon IFN-γ pre-treatment. Since patients' AML blasts are rare…

0301 basic medicineCD4-Positive T-LymphocytesCytotoxicity ImmunologicCancer ResearchAdoptive cell transferGenotypemedicine.medical_treatmentHematopoietic stem cell transplantationBiologyLymphocyte ActivationImmunotherapy Adoptive03 medical and health sciencesMice0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansTransplantation HomologousAllelesHLA-DP beta-ChainsLeukemiaHematopoietic Stem Cell TransplantationMyeloid leukemiaHematologyImmunotherapymedicine.diseaseTissue DonorsTransplantationCTL*LeukemiaLeukemia Myeloid Acute030104 developmental biologyOncologyImmunologyFemaleImmunotherapyStem cell030215 immunologyLeukemia
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Patient-individualized CD8+cytolytic T-cell therapy effectively combats minimal residual leukemia in immunodeficient mice

2015

Adoptive transfer of donor-derived cytolytic T-lymphocytes (CTL) has evolved as a promising strategy to improve graft-versus-leukemia (GvL) effects in allogeneic hematopoietic stem-cell transplantation. However, durable clinical responses are often hampered by limited capability of transferred T cells to establish effective and sustained antitumor immunity in vivo. We therefore analyzed GvL responses of acute myeloid leukemia (AML)-reactive CD8(+) CTL with central and effector memory phenotype in a new allogeneic donor-patient specific humanized mouse model. CTL lines and clones obtained upon stimulation of naive CD45RA(+) donor CD8(+) T cells with either single HLA antigen-mismatched or HL…

0301 basic medicineCancer ResearchAdoptive cell transferbusiness.industryT cellMyeloid leukemiamedicine.diseaseMinimal residual disease03 medical and health sciencesCTL*Leukemia030104 developmental biologymedicine.anatomical_structureOncologyhemic and lymphatic diseasesHumanized mouseImmunologyMedicineBone marrowbusinessInternational Journal of Cancer
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Common extracellular matrix regulation of myeloid cell activity in the bone marrow and tumor microenvironments

2017

The complex interaction between cells undergoing transformation and the various stromal and immunological cell components of the tumor microenvironment (TME) crucially influences cancer progression and diversification, as well as endowing clinical and prognostic significance. The immunosuppression characterizing the TME depends on the recruitment and activation of different cell types including regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. Less considered is the non-cellular component of the TME. Here, we focus on the extracellular matrix (ECM) regulatory activities that, within the TME, actively contribute to many aspects of tumor progression, acti…

0301 basic medicineCancer ResearchCell typeStromal cellMyeloidCarcinogenesisImmunologyBiology03 medical and health sciencesBone MarrowNeoplasmsmedicineImmune ToleranceImmunology and AllergyAnimalsHumansMyeloid-Derived Suppressor CellCarcinogenesiTumor microenvironmentAnimalMyeloid-Derived Suppressor CellsHematopoietic stem cellSPARCBone marrow nicheExtracellular matrixCell biology030104 developmental biologymedicine.anatomical_structureRegulatory myeloid suppressor cellOncologyTumor microenvironmentTumor progressionMyeloid-derived Suppressor CellBone marrow niche; Extracellular matrix; Regulatory myeloid suppressor cells; SPARC; Tumor microenvironment; Animals; Bone Marrow; Carcinogenesis; Extracellular Matrix; Humans; Immune Tolerance; Myeloid-Derived Suppressor Cells; Neoplasms; Tumor Escape; Tumor MicroenvironmentNeoplasmTumor Escapesense organsBone marrowHuman
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Tumor-Derived Prostaglandin E2 Promotes p50 NF-κB-Dependent Differentiation of Monocytic MDSCs

2020

Abstract Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to suppress adaptive immunity and to hinder the effectiveness of anticancer treatments. Of note, in response to IFNγ, M-MDSCs release the tumor-promoting and immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-κB in M-MDSCs, diverting their response to IFNγ toward NO-mediated immunosuppression and reducing TNFα expression. At the genome level, p50 NF-κB promoted binding …

0301 basic medicineCancer ResearchCellular differentiationProstaglandin E2 receptormedicine.medical_treatmentMelanoma ExperimentalApoptosisSettore MED/08 - Anatomia PatologicaNitric OxideDinoprostoneMonocytesInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemOxytocicsImmune ToleranceTumor Cells CulturedmedicineAnimalsHumansProstaglandin E2Cell ProliferationChemistryMyeloid-Derived Suppressor CellsNF-kappa B p50 SubunitCell DifferentiationImmunotherapyAcquired immune systemPancreatic Neoplasms030104 developmental biologyOncologyp50 NF-κB differentiation of monocytic MDSC.030220 oncology & carcinogenesisMyeloid-derived Suppressor CellCancer researchTumor necrosis factor alphaColorectal Neoplasmsmedicine.drugCancer Research
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Targeting the chromosomal passenger complex subunit INCENP induces polyploidization, apoptosis and senescence in neuroblastoma

2019

Abstract Chromosomal passenger complex (CPC) has been demonstrated to be a potential target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer including neuroblastoma. However, chemical inhibition of either Aurora B or survivin does not target CPC specifically due to off-target effects or CPC-independent activities of these two components. In a previous chromatin-focused siRNA screen, we found that neuroblastoma cells were particularly vulnerable to loss of INCENP, a gene encoding a key scaffolding component of the CPC. In this study, INCENP was highly expressed by neuroblastoma cells, and its expression decreased following retinoic acid–induced neuroblastoma …

0301 basic medicineCancer ResearchINCENP/CPC/Polyploidy/DNA damage/Apoptosis/SenescenceCarcinogenesisChromosomal Proteins Non-HistoneAurora B kinaseApoptosisBiologymedicine.disease_causeArticlePolyploidy03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaSurvivinmedicineGene silencingAnimalsHumansneoplasmsCellular SenescenceINCENPmedicine.disease030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer researchHeterograftsCarcinogenesis
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Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis

2017

Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H2O2 triggers genome-wide DNA mutations in intestinal epithelial cells to stimulate invasive growth. Moreover, increased reactive oxygen species (ROS) production in myeloid cells initiates tumor growth in various organs also in the absence of a carcinogen challenge in a paracrine manner. Our data identify an i…

0301 basic medicineCancer ResearchMyeloidDNA damageApoptosismedicine.disease_causeMice03 medical and health sciencesParacrine signallingmedicineAnimalsMyeloid Cellschemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentChemistryEpithelial CellsHydrogen PeroxideCell BiologyMice Mutant StrainsCell biologyOxidative Stress030104 developmental biologymedicine.anatomical_structureOncologyMutagenesisMutationTumor necrosis factor alphaReactive Oxygen SpeciesCarcinogenesisOxidative stressDNA DamageSignal TransductionCancer Cell
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Bacitracin and Rutin Regulate Tissue Factor Production in Inflammatory Monocytes and Acute Myeloid Leukemia Blasts

2021

Simple Summary Aberrant tissue factor (TF) expression by transformed myeloblasts and inflammatory monocytes contributes to coagulation activation in acute myeloid leukemia (AML). TF procoagulant activity (PCA) is regulated by protein disulfide isomerase (PDI), an oxidoreductase with chaperone activity, but its specific role in AML-associated TF biology is unclear. Here, we provide novel mechanistic insights into this interrelation. We show that bacitracin and rutin, two pan-inhibitors of the PDI family, prevent lipopolysaccharide (LPS)-induced monocyte TF production under inflammatory conditions and constitutive TF expression by THP1 cells and AML blasts, thus exerting promising anticoagula…

0301 basic medicineCancer ResearchMyeloidDaunorubicinacute myeloid leukemia030204 cardiovascular system & hematologyPeripheral blood mononuclear cellArticleFlow cytometry03 medical and health sciencesTissue factor0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesmedicinecoagulationProtein disulfide-isomeraseRC254-282medicine.diagnostic_testChemistryrutinNeoplasms. Tumors. Oncology. Including cancer and carcinogensMyeloid leukemiatissue factorprotein disulfide isomeraseMolecular biology030104 developmental biologymedicine.anatomical_structureOncologyinflammationtissue factor; protein disulfide isomerase; acute myeloid leukemia; coagulation; inflammation; rutin; monocytesmonocytesmedicine.drugCancers
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