Search results for " regulatory"

showing 10 items of 556 documents

Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice

2019

The CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interle…

0301 basic medicineApolipoprotein Emedicine.medical_specialtyRegulatory T cellCCL1030204 cardiovascular system & hematologyCCR8T-Lymphocytes RegulatoryReceptors CCR8Chemokine CCL1Mice03 medical and health sciencesApolipoproteins ETh2 Cells0302 clinical medicineInternal medicineLeukocytesmedicineSplenocyteAnimalsMolecular BiologyInflammationMice KnockoutChemistryTh1 CellsAtherosclerosisInterleukin-10Mice Inbred C57BLTregInterleukin 10030104 developmental biologyEndocrinologymedicine.anatomical_structureIL-10CytokinesCardiology and Cardiovascular MedicineCCR8Intravital microscopyCCL1LipoproteinJournal of Molecular and Cellular Cardiology
researchProduct

Progranulin overexpression in sensory neurons attenuates neuropathic pain in mice: Role of autophagy

2016

Peripheral or central nerve injury is a frequent cause of chronic pain and the mechanisms are not fully understood. Using newly generated transgenic mice we show that progranulin overexpression in sensory neurons attenuates neuropathic pain after sciatic nerve injury and accelerates nerve healing. A yeast-2-hybrid screen revealed putative interactions of progranulin with autophagy-related proteins, ATG12 and ATG4b. This was supported by colocalization and proteomic studies showing regulations of ATG13 and ATG4b and other members of the autophagy network, lysosomal proteins and proteins involved in endocytosis. The association of progranulin with the autophagic pathway was functionally confi…

0301 basic medicineAutophagy-Related ProteinsMiceProgranulinsGanglia SpinalDorsal root gangliaGranulinsPain MeasurementCD11b AntigenMicrofilament ProteinsChronic painSciatic nerve injuryCysteine Endopeptidasesmedicine.anatomical_structureNociceptionNeurologyNeuropathic painIntercellular Signaling Peptides and Proteinsmedicine.symptomMicrotubule-Associated ProteinsNerve injuryProgranulinSensory Receptor CellsGreen Fluorescent ProteinsPainMice Transgeniclcsh:RC321-571ATG1203 medical and health sciencesLysosomal-Associated Membrane Protein 1mental disordersmedicineAutophagyAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryActivating Transcription Factor 3Sensory neuronbusiness.industryAutophagyCalcium-Binding ProteinsNerve injurymedicine.diseaseSensory neuronMice Inbred C57BLDisease Models Animal030104 developmental biologyGene OntologyNeuralgiabusinessApoptosis Regulatory ProteinsNeuroscienceNeurobiology of Disease
researchProduct

Dynamics and predicted drug response of a gene network linking dedifferentiation with β-catenin dysfunction in hepatocellular carcinoma

2019

Background & Aims Alterations of individual genes variably affect the development of hepatocellular carcinoma (HCC). Thus, we aimed to characterize the function of tumor-promoting genes in the context of gene regulatory networks (GRNs). Methods Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer – RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1). We further generated and validated a quantitative mathematical model of the GRN using human cell lines and in vivo expression data. Results We found that LIN28B and C…

0301 basic medicineBeta-cateninCarcinoma HepatocellularHepatocellular carcinomaLIN28BCellGene regulatory networkPrincipal component analysisMice TransgenicBiologyTransfectionTranscriptomeCohort Studies03 medical and health sciencesMice0302 clinical medicineMathematical modelmicroRNAmedicineAnimalsHumansGene Regulatory NetworksCTNNB1Genebeta CateninHepatologySequence Analysis RNALiver NeoplasmsGene regulatory networkRNA-Binding ProteinsHGF/MET pathwayMicroRNAHep G2 CellsHCCSModels TheoreticalPrognosisPersonalized medicinedigestive system diseases030104 developmental biologymedicine.anatomical_structureCancer researchSMARCA4biology.protein030211 gastroenterology & hepatologyTranscriptome
researchProduct

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
researchProduct

Reciprocal regulation of the Il9 locus by counteracting activities of transcription factors IRF1 and IRF4.

2017

The T helper 9 (Th9) cell transcriptional network is formed by an equilibrium of signals induced by cytokines and antigen presentation. Here we show that, within this network, two interferon regulatory factors (IRF), IRF1 and IRF4, display opposing effects on Th9 differentiation. IRF4 dose-dependently promotes, whereas IRF1 inhibits, IL-9 production. Likewise, IRF1 inhibits IL-9 production by human Th9 cells. IRF1 counteracts IRF4-driven Il9 promoter activity, and IRF1 and IRF4 have opposing function on activating histone modifications, thus modulating RNA polymerase II recruitment. IRF1 occupancy correlates with decreased IRF4 abundance, suggesting an IRF1-IRF4-binding competition at the I…

0301 basic medicineCD4-Positive T-LymphocytesScienceCellular differentiationAntigen presentationGeneral Physics and AstronomyRNA polymerase IIMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsHumansInterleukin 9Transcription factorMice KnockoutMultidisciplinaryGene Expression ProfilingQInterleukin-9Cell DifferentiationGeneral ChemistryT-Lymphocytes Helper-InducerCell biologyMice Inbred C57BL030104 developmental biologyIRF1Interferon Regulatory Factorsbiology.protein030215 immunologyInterferon regulatory factorsmedicine.drugInterferon Regulatory Factor-1Nature communications
researchProduct

Expression of regulatory genes in the embryonic brain of a lizard and implications for understanding pallial organization and evolution

2017

The comparison of gene expression patterns in the embryonic brain of mouse and chicken is being essential for understanding pallial organization. However, the scarcity of gene expression data in reptiles, crucial for understanding evolution, makes it difficult to identify homologues of pallial divisions in different amniotes. We cloned and analyzed the expression of the genes Emx1, Lhx2, Lhx9, and Tbr1 in the embryonic telencephalon of the lacertid lizard Psammodromus algirus. The comparative expression patterns of these genes, critical for pallial development, are better understood when using a recently proposed six-part model of pallial divisions. The lizard medial pallium, expressing all…

0301 basic medicineCalbindinsArcopalliumLIM-Homeodomain ProteinsEMX1ReptileBiologyCalbindinLhx903 medical and health sciencesforebrain evolutiontranscription factorsmedicineTranscription factorsAnimalsDlx2Research ArticlesHomeodomain ProteinsNeocortexCerebrumGeneral NeuroscienceDLX2RRID AB_10000340BrainGene Expression Regulation DevelopmentalLizardsBiological Evolutionreptile030104 developmental biologymedicine.anatomical_structureCalbindin 1Developmental regulatory genesbiology.proteinNidopalliumEmx1TBR1developmental regulatory genesT-Box Domain ProteinsNeuroscienceForebrain evolutionResearch Article
researchProduct

Caloric Restriction Mimetics Enhance Anticancer Immunosurveillance

2016

International audience; Caloric restriction mimetics (CRMs) mimic the biochemical effects of nutrient deprivation by reducing lysine acetylation of cellular proteins, thus triggering autophagy. Treatment with the CRM hydroxycitrate, an inhibitor of ATP citrate lyase, induced the depletion of regulatory T cells (which dampen anticancer immunity) from autophagy-competent, but not autophagy-deficient, mutant KRAS-induced lung cancers in mice, thereby improving anticancer immunosurveillance and reducing tumor mass. Short-term fasting or treatment with several chemically unrelated autophagy-inducing CRMs, including hydroxycitrate and spermidine, improved the inhibition of tumor growth by chemoth…

0301 basic medicineCancer ResearchATP citrate lyaseSpermidineBariatric SurgeryimmunosurveillanceT-Lymphocytes RegulatoryAutophagy-Related Protein 5[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compoundMiceregulatory T cellCitrates3. Good healthImmunogenic Cell-DeathImmunosurveillancemedicine.anatomical_structureOncologyBiochemistryDifferentiationembryonic structuresImmunogenic cell deathIn-VivoHumanRegulatory T cell[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyDietary RestrictionNOProto-Oncogene Proteins p21(ras)03 medical and health sciencesMonitoring ImmunologicIn vivoCell Line TumormedicineAutophagyAnimalsHumanscancerChemotherapyBreast-CancerCaloric Restrictioncancer; chemotherapy immunosurveillance regulatory T cellAnimal[ SDV.BC ] Life Sciences [q-bio]/Cellular Biologyregulatory T&nbspAutophagyfungiNeoplasms ExperimentalcellSpermidineMethotrexate030104 developmental biologychemistryAcetylationMutationCancer researchCitrateNeoplasm Transplantation
researchProduct

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
researchProduct

The phospholipase DDHD1 as a new target in colorectal cancer therapy

2018

Background Our previous study demonstrates that Citrus-limon derived nanovesicles are able to decrease colon cancer cell viability, and that this effect is associated with the downregulation of the intracellular phospholipase DDHD domain-containing protein 1 (DDHD1). While few studies are currently available on the contribution of DDHD1 in neurological disorders, there is no information on its role in cancer. This study investigates the role of DDHD1 in colon cancer. Methods DDHD1 siRNAs and an overexpression vector were transfected into colorectal cancer and normal cells to downregulate or upregulate DDHD1 expression. In vitro and in vivo assays were performed to investigate the functional…

0301 basic medicineCancer ResearchColorectal cancerApoptosisMiceSettore BIO/13 - Biologia ApplicataGene Regulatory NetworksMolecular Targeted TherapyCitrus-limon nanovesicleTransfectionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Oncology; Cancer ResearchOncologyPhospholipasesCitrus-limon nanovesicles; Colorectal cancer; Phospholipase DDHD1; Animals; Antineoplastic Agents; Apoptosis; Cell Line Tumor; Cell Proliferation; Colorectal Neoplasms; Computational Biology; Disease Models Animal; Female; Gene Expression Profiling; Gene Ontology; Gene Regulatory Networks; Gene Silencing; Humans; MAP Kinase Signaling System; Mice; Phospholipases; Signal Transduction; Xenograft Model Antitumor Assays; Biomarkers Tumor; Molecular Targeted TherapyFemaleColorectal NeoplasmsSignal TransductionMAP Kinase Signaling SystemAntineoplastic Agentslcsh:RC254-282Citrus-limon nanovesicles03 medical and health sciencesDownregulation and upregulationIn vivoCell Line TumorBiomarkers TumormedicineAnimalsHumansGene silencingGene SilencingPhospholipase DDHD1Cell Proliferationbusiness.industryCell growthGene Expression ProfilingResearchComputational BiologyCancermedicine.diseaseXenograft Model Antitumor AssaysColorectal cancerDisease Models AnimalGene Ontology030104 developmental biologyApoptosisCancer researchbusiness
researchProduct

PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
researchProduct