Search results for "Cytokine Signaling"

showing 10 items of 22 documents

NAFLD and Atherosclerosis Are Prevented by a Natural Dietary Supplement Containing Curcumin, Silymarin, Guggul, Chlorogenic Acid and Inulin in Mice F…

2017

Non-alcoholic fatty liver disease (NAFLD) confers an increased risk of cardiovascular diseases. NAFDL is associated with atherogenic dyslipidemia, inflammation and renin-angiotensin system (RAS) imbalance, which in turn lead to atherosclerotic lesions. In the present study, the impact of a natural dietary supplement (NDS) containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin on NAFLD and atherosclerosis was evaluated, and the mechanism of action was examined. C57BL/6 mice were fed an HFD for 16 weeks; half of the mice were simultaneously treated with a daily oral administration (os) of the NDS. NAFLD and atherogenic lesions in aorta and carotid artery (histological analys…

0301 basic medicineMaleAngiotensinogenAdministration OralSettore BIO/09 - Fisiologiachemistry.chemical_compoundMice0302 clinical medicineNon-alcoholic Fatty Liver DiseasePlant GumsCommiphorachemistry.chemical_classificationNutrition and Dieteticsnon-alcoholic fatty liver disease; atherogenic lesions; diet-induced obesity; natural dietary supplement; renin-angiotensin system imbalance; Profiler PCR arrayAngiotensin IIFatty liverInulinNeoplasm Proteinsrenin-angiotensin system imbalance030211 gastroenterology & hepatologyatherogenic lesionmedicine.symptomChlorogenic AcidSilymarinmedicine.medical_specialtynatural dietary supplementCurcumindiet-induced obesityProfiler PCR array; atherogenic lesions; diet-induced obesity; natural dietary supplement; non-alcoholic fatty liver disease; renin-angiotensin system imbalanceInflammationBiologyDiet High-FatFatty Acid-Binding ProteinsArticle03 medical and health sciencesInternal medicineRenin–angiotensin systemmedicineAnimalsRNA MessengerProfiler PCR arrayatherogenic lesionsPlant ExtractsFatty acidLipid metabolismmedicine.diseaseAtherosclerosisLipid MetabolismMice Inbred C57BL030104 developmental biologyEndocrinologychemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinDietary SupplementsCurcuminSteatosisDyslipidemiaFood ScienceNutrients
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A Systematic Study of Dysregulated MicroRNA in Type 2 Diabetes Mellitus

2017

MicroRNAs (miRNAs) are small noncoding RNAs that modulate the cellular transcriptome at the post-transcriptional level. miRNA plays important roles in different disease manifestation, including type 2 diabetes mellitus (T2DM). Many studies have characterized the changes of miRNAs in T2DM, a complex systematic disease; however, few studies have integrated these findings and explored the functional effects of the dysregulated miRNAs identified. To investigate the involvement of miRNAs in T2DM, we obtained and analyzed all relevant studies published prior to 18 October 2016 from various literature databases. From 59 independent studies that met the inclusion criteria, we identified 158 dysregu…

0301 basic medicineSystematic surveytype 2 diabetes mellitussystematic study030209 endocrinology & metabolismDiseaseBioinformaticsCatalysisArticleInorganic ChemistryTranscriptomelcsh:Chemistry03 medical and health sciences0302 clinical medicineDiabetes mellitusmiRNA-mRNA interaction networkmicroRNAmedicineHumansGene Regulatory NetworksRNA MessengerPhysical and Theoretical Chemistry10. No inequalityMolecular Biologylcsh:QH301-705.5SpectroscopyAdipocytokine Signaling PathwaymicroRNA; type 2 diabetes mellitus; miRNA-mRNA interaction network; systematic studymicroRNAbusiness.industryGene Expression ProfilingOrganic ChemistryType 2 Diabetes MellitusGeneral Medicinemedicine.diseaseComputer Science ApplicationsMicroRNAs030104 developmental biologyDiabetes Mellitus Type 2Gene Expression Regulationlcsh:Biology (General)lcsh:QD1-999Organ SpecificityRNA InterferenceDisease manifestationbusinessTranscriptomeSignal TransductionInternational Journal of Molecular Sciences
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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis

2018

Background & Aims The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice. Methods We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from tr…

0301 basic medicineTranscription FactorBiopsyInbred C57BLTransgenicImmune RegulationSettore MED/12MiceRandom Allocation0302 clinical medicineCrohn DiseaseReference ValuesNeedleIntestinal Mucosaintegumentary systemChemistryBiopsy NeedleGastroenterologyT helper cellFlow CytometryPost-translational ModificationImmunohistochemistryDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structure030211 gastroenterology & hepatologyTumor necrosis factor alphaSignal TransductionGenetically modified mouseRegulatory T cellTransgeneMice TransgenicSmad7 ProteinTransforming Growth Factor beta103 medical and health sciencesImmune systemmedicineAnimalsHumansCytokine SignalingHepatologyAnimalHEK 293 cellsUbiquitinationMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyDisease ModelsCytokine Signaling; Immune Regulation; Post-translational Modification; Transcription Factor; Biopsy Needle; Crohn Disease; Cysteine Endopeptidases; Deubiquitinating Enzyme CYLD; Disease Models Animal; Flow Cytometry; Immunohistochemistry; Intestinal Mucosa; Mice Inbred C57BL; Mice Transgenic; Random Allocation; Reference Values; Signal Transduction; Smad7 Protein; Transforming Growth Factor beta1; UbiquitinationTransforming growth factorGastroenterology
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Mucosal immunoregulation: transcription factors as possible therapeutic targets.

2005

Much progress has been recently made with regard to our understanding of the mucosal immune system in health and disease. In particular, it has been shown that uncontrolled mucosal immune responses driven by lymphocytes or non-lymphoid cells may lead to immunological diseases such as allergy, hypersensitivity and inflammation. Thus, a more detailed understanding of mucosal immune regulation and decision making at mucosal surfaces is essential for a better understanding of mucosal immune responses in health and disease. Antigen presenting cells and T lymphocytes play a key role in controlling mucosal immune responses. To deal with this key task, T helper cells differentiate into functionally…

AllergyImmunologyInflammationApoptosisSuppressor of Cytokine Signaling ProteinsAllergic inflammationPathogenesisImmune systemImmunitymedicineHypersensitivityImmunology and AllergyAnimalsHumansIL-2 receptorMast CellsAntigen-presenting cellGlucocorticoidsImmunity MucosalPharmacologybusiness.industrymedicine.diseaseInflammatory Bowel DiseasesAsthmaIntestinesSuppressor of Cytokine Signaling 3 ProteinImmunologyCytokinesmedicine.symptombusinessTranscription FactorsCurrent drug targets. Inflammation and allergy
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SOCS3 transactivation by PPARγ prevents IL-17-driven cancer growth.

2013

Abstract Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely characterized. Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARγ. SOCS3 promoter binding and gene transactivation by PPARγ was associated with a repression in differentiation of proinflammatory T-helper (TH)17 cells. Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARγ by DHA. Furthermore, naïve CD4…

CD4-Positive T-LymphocytesCancer ResearchAngiogenesisMammary Neoplasms Experimental/genetics/pathology/prevention & controlSuppressor of Cytokine Signaling Proteinsddc:616.07BioinformaticsTransactivationMice0302 clinical medicineTumor Burden/drug effects/geneticsSOCS3Docosahexaenoic Acids/administration & dosage/pharmacologyPromoter Regions GeneticMice Knockout0303 health sciencesMice Inbred BALB CChemistryReverse Transcriptase Polymerase Chain ReactionInterleukin-17InterleukinCell DifferentiationCell biologyTumor BurdenOncology030220 oncology & carcinogenesisFemaleRNA InterferenceInterleukin 17Th17 Cells/drug effects/metabolismTranscriptional ActivationDocosahexaenoic AcidsBlotting WesternMice NudeCD4-Positive T-Lymphocytes/drug effects/metabolismProinflammatory cytokine03 medical and health sciencesSuppressor of Cytokine Signaling Proteins/genetics/metabolismCell Line TumorAnimalsTranscription factor030304 developmental biologyMammary Neoplasms ExperimentalPromoter Regions Genetic/geneticsDietMice Inbred C57BLPPAR gammaInterleukin-17/metabolismCell cultureSuppressor of Cytokine Signaling 3 ProteinCell Differentiation/drug effectsPPAR gamma/agonists/genetics/metabolismTh17 CellsCancer research
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Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

2005

Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

Cancer ResearchLymphoma B-Cellbusiness.industrySuppressor of cytokine signaling 1HomozygoteIntracellular Signaling Peptides and ProteinsSuppressor of Cytokine Signaling ProteinsHematologymedicine.diseaseMediastinal NeoplasmsLymphomaRepressor ProteinsSuppressor of Cytokine Signaling 1 ProteinOncologyhemic and lymphatic diseasesmedicineCancer researchHumansPrimary mediastinal B-cell lymphomaDNA microarraybusinessGene DeletionOligonucleotide Array Sequence AnalysisLeukemia
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SOCS2 controls proliferation and stemness of hematopoietic cells under stress conditions and its deregulation marks unfavorable acute leukemias

2015

Abstract Hematopoietic stem cells (HSC) promptly adapt hematopoiesis to stress conditions, such as infection and cancer, replenishing bone marrow–derived circulating populations, while preserving the stem cell reservoir. SOCS2, a feedback inhibitor of JAK–STAT pathways, is expressed in most primitive HSC and is upregulated in response to STAT5-inducing cytokines. We demonstrate that Socs2 deficiency unleashes HSC proliferation in vitro, sustaining STAT5 phosphorylation in response to IL3, thrombopoietin, and GM-CSF. In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marro…

Cancer ResearchMyeloidSuppressor of Cytokine Signaling ProteinsMice TransgenicNeoplasm ProteinMiceBone MarrowSuppressor of Cytokine Signaling ProteinmedicineAnimalsHumansMEF2 Transcription FactorThrombopoietinSTAT5Cell ProliferationRegulation of gene expressionABLLeukemiabiologyMEF2 Transcription FactorsAnimalMedicine (all)Animals; Bone Marrow; Cell Differentiation; Cell Proliferation; Fluorouracil; Gene Expression Regulation Neoplastic; Hematopoietic Stem Cells; Humans; Leukemia; MEF2 Transcription Factors; Mice; Mice Transgenic; Neoplasm Proteins; Neoplastic Stem Cells; Suppressor of Cytokine Signaling Proteins; Cancer Research; Oncology; Medicine (all)breakpoint cluster regionCell DifferentiationHematopoietic Stem CellHematopoietic Stem CellsNeoplasm ProteinsGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinCancer researchNeoplastic Stem CellsFluorouracilNeoplastic Stem CellStem cellHuman
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
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OTUB1 inhibits CNS autoimmunity by preventing IFN-γ-induced hyperactivation of astrocytes.

2019

Astrocytes are critical regulators of neuroinflammation in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Growing evidence indicates that ubiquitination of signaling molecules is an important cell‐intrinsic mechanism governing astrocyte function during MS and EAE. Here, we identified an upregulation of the deubiquitinase OTU domain, ubiquitin aldehyde binding 1 (OTUB1) in astrocytes during MS and EAE. Mice with astrocyte‐specific OTUB1 ablation developed more severe EAE due to increased leukocyte accumulation, proinflammatory gene transcription, and demyelination in the spinal cord as compared to control mice. OTUB1‐deficient astrocytes were hy…

Central Nervous SystemEncephalomyelitis Autoimmune ExperimentalNeuroimmunomodulationmedicine.medical_treatmentexperimental autoimmune encephalomyelitisAutoimmunityBiologymultiple sclerosisubiquitinationGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineastrocytemedicineAnimalsMolecular BiologyCells CulturedNeuroinflammation030304 developmental biologyMice Knockout0303 health sciencesGeneral Immunology and MicrobiologySuppressor of cytokine signaling 1General NeuroscienceExperimental autoimmune encephalomyelitisArticlesmedicine.disease3. Good healthCell biologyMice Inbred C57BLCysteine EndopeptidasesCytokinemedicine.anatomical_structureAnimals NewbornAstrocytesSTAT proteinOTUB1FemaleNeurogenic InflammationJanus kinase030217 neurology & neurosurgeryAstrocyte
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