Search results for " ACTIVATION"

showing 10 items of 1535 documents

Human apolipoprotein A-I Gly26Arg stimulation of inflammatory responses via NF-kB activation: Potential roles in amyloidosis?

2018

The cascade of molecular events leading to Human apolipoprotein A–I (apoA–I) amyloidosis is not completely understood, not even the pathways that determine clinical manifestations associated to systemic protein deposition in organs such as liver, kidney and heart. About twenty natural variants of apoA–I were described as inducing amyloidosis, but the mechanisms driving their aggregation and deposition are still unclear. We previously identified that the mutant Gly26Arg but not Lys107-0 induced the release of cytokines and reactive oxygen species from cultured RAW 264.7 murine macrophages, suggesting that part of the pathogenic pathway could elicit of an inflammatory signal. In this work we …

0301 basic medicineLipopolysaccharideMACROPHAGES ACTIVATIONMutantStimulationInflammationOxidative phosphorylationPathology and Forensic MedicineCiencias Biológicas03 medical and health scienceschemistry.chemical_compoundINFLAMMATIONPhysiology (medical)APOLIPOPROTEIN A-I VARIANTSmedicineNUCLEAR FACTOR-ΚBchemistry.chemical_classificationReactive oxygen speciesAmyloidosisNF-κBBioquímica y Biología Molecularmedicine.diseaseCell biology030104 developmental biologychemistryAMYLOIDOSISlipids (amino acids peptides and proteins)medicine.symptomCIENCIAS NATURALES Y EXACTASPathophysiology
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Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
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In Vivo siRNA Delivery to Immunosuppressive Liver Macrophages by alpha-Mannosyl-Functionalized Cationic Nanohydrogel Particles

2020

Macrophages are the front soldiers of the innate immune system and are vital for immune defense, tumor surveillance, and tissue homeostasis. In chronic diseases, including cancer and liver fibrosis, macrophages can be forced into an immunosuppressive and profibrotic M2 phenotype. M2-type macrophages overexpress the mannose receptor CD206. Targeting these cells via CD206 and macrophage repolarization towards an immune stimulating and antifibrotic M1 phenotype through RNA interference represents an appealing therapeutic approach. We designed nanohydrogel particles equipped with mannose residues on the surface (ManNP) that delivered siRNA more efficiently to M2 polarized macrophages compared t…

0301 basic medicineLiver CirrhosissiRNA deliveryTHP-1 Cellsmedicine.medical_treatmentmannose targetingMice0302 clinical medicineDrug Delivery SystemsFibrosisMacrophageM2 macrophagesRNA Small Interferinglcsh:QH301-705.5Tissue homeostasisMice Inbred BALB CChemistryHydrogelsGeneral MedicineHep G2 CellsLiver030220 oncology & carcinogenesisFemaleimmunotherapyMannose receptorMannose ReceptorReceptors Cell Surfacegene knock-downArticlenanohydrogels03 medical and health sciencesImmune systemIn vivomedicineImmune ToleranceAnimalsHumanscancerLectins C-TypeInnate immune systemMacrophagesfibrosisImmunotherapyMacrophage Activationmedicine.disease030104 developmental biologyMannose-Binding LectinsRAW 264.7 Cellslcsh:Biology (General)Cancer researchNanoparticlesMannose
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Ellagitannin-rich cloudberry inhibits hepatocyte growth factorinduced cell migration and phosphatidylinositol 3-kinase/AKT activation in colon carcin…

2016

// Anne-Maria Pajari 1, 2 , Essi Paivarinta 1 , Lassi Paavolainen 3 , Elina Vaara 1 , Tuuli Koivumaki 4 , Ritu Garg 5 , Anu Heiman-Lindh 1 , Marja Mutanen 1 , Varpu Marjomaki 3 , Anne J. Ridley 2, 5 1 Department of Food and Environmental Sciences, Division of Nutrition, University of Helsinki, Helsinki, Finland 2 University College London, Ludwig Institute for Cancer Research, London, UK 3 Department of Biological and Environmental Science / Nanoscience Center, University of Jyvaskyla, Jyvaskyla, Finland 4 Department of Food and Environmental Sciences, Division of Food Chemistry, University of Helsinki, Helsinki, Finland 5 Randall Division of Cell & Molecular Biophysics, King’s College Lond…

0301 basic medicineMAPK/ERK pathwaycell migrationColorectal cancerCellMetastasisMicePhosphatidylinositol 3-Kinases0302 clinical medicineCell MovementHepatocyte Growth FactorHydrolyzable Tanninsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisColonic NeoplasmsHepatocyte growth factormedicine.drugResearch PapersolumigraatioAntineoplastic Agentscolorectal cancerMet receptorAdenocarcinoma03 medical and health sciencesCell Line TumorellagitanninsmedicineJournal ArticleAnimalsHumansCell migrationProtein kinase Bbusiness.industryPlant Extractsta1182Cancerta3122medicine.diseaseMice Mutant StrainsMin mouseEnzyme ActivationMice Inbred C57BL030104 developmental biologyCancer cellImmunologyCancer researchbusinessRubusProto-Oncogene Proteins c-akt
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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Visualizing Leukocyte Rolling and Adhesion in Angiotensin II-Infused Mice: Techniques and Pitfalls

2018

Epifluorescence intravital video microscopy (IVM) of blood vessels is an established method to evaluate the activation of immune cells and their ability to role and adhere to the endothelial layer. Visualization of circulating cells by injection of fluorescent dyes or fluorophore-coupled antibodies is commonly used. Alternatively, fluorescent reporter mice can be used. Interactions of leukocytes, in particular lysozyme M+ (LysM+) monocytes, with the vessel wall play pivotal roles in promoting vascular dysfunction and arterial hypertension. We here present the technique to visualize and quantify leukocyte rolling and adhesion in carotid arteries in angiotensin II (AngII)-induced hypertension…

0301 basic medicineMaleEndotheliumendotheliumGeneral Chemical EngineeringImmunologyLeukocyte RollingMice TransgenicMonocytesGeneral Biochemistry Genetics and Molecular BiologyGreen fluorescent protein03 medical and health scienceschemistry.chemical_compoundMiceintravital microscopymedicineacridine orangeCell AdhesionLeukocytesAnimalsLeukocyte RollingCell adhesionGeneral Immunology and Microbiologycarotid arteryAngiotensin IIGeneral NeuroscienceAcridine orangeAngiotensin IICell biologyIssue 131030104 developmental biologymedicine.anatomical_structureCarotid ArterieschemistryHypertensioncardiovascular systemdouble-fluorescent Cre reporter mouseCell activationIntravital microscopyJournal of Visualized Experiments
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Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators

2016

The fatigue induced by marathon races was observed in terms of inflammatory and immunological outcomes. Neutrophil survival and activation are essential for inflammation resolution and contributes directly to the pathogenesis of many infectious and inflammatory conditions. The aim of this study was to investigate the effect of marathon races on surface molecules related to neutrophil adhesion and extrinsic apoptosis pathway and its association with inflammatory markers. We evaluated 23 trained male runners at the Sao Paulo International Marathon 2013. The following components were measured: hematological and inflammatory mediators, muscle damage markers, and neutrophil function. The maratho…

0301 basic medicineMaleNeutrophilsPhysiologylcsh:MedicineApoptosisDNA fragmentationPathology and Laboratory MedicineBiochemistryNeutrophil ActivationRunningPathogenesischemistry.chemical_compoundWhite Blood CellsLeukocyte Count0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinarybiologyCell DeathInterleukinHematologyFas receptorBody FluidsNucleic acidsBloodHematocritCell ProcessesAntigens SurfaceCytokinesTumor necrosis factor alphamedicine.symptomCellular TypesAnatomyInflammation MediatorsResearch ArticleAdultCell SurvivalImmune CellseducationImmunologyInflammation03 medical and health sciencesSigns and SymptomsDiagnostic MedicineLactate dehydrogenasemedicineGeneticsHumansLeukocyte RollingHemoglobinInflammationBlood Cellsbusiness.industrylcsh:RBiology and Life SciencesProteins030229 sport sciencesCell BiologyDNAMolecular DevelopmentBlood Counts030104 developmental biologychemistryApoptosisImmune SystemImmunologybiology.proteinCreatine kinaselcsh:Qbusinesshuman activitiesDevelopmental BiologyPLoS ONE
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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Functional role of endothelial CXCL16/CXCR6-platelet-leucocyte axis in angiotensin II-associated metabolic disorders.

2018

Aims Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leucocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signalling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders. Methods and results Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leucocyte adhesion to arterial but not to venous endothelial cells. Flow cytometry and immunofluorescence s…

0301 basic medicineMaleRHOAPhysiologyMice Knockout ApoE030204 cardiovascular system & hematology0302 clinical medicineLeukocytesReceptorCells CulturedMetabolic SyndromebiologyChemistryAngiotensin IIMiddle AgedAortic AneurysmVascular endothelial growth factor ALosartanmedicine.anatomical_structurecardiovascular systemFemaleCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionAdultBlood Plateletsmedicine.medical_specialtyEndothelium03 medical and health sciencesPhysiology (medical)Internal medicinemedicineCell AdhesionAnimalsHumansPlatelet activationReceptors CXCR6Angiotensin II receptor type 1Endothelial CellsChemokine CXCL16Platelet ActivationAngiotensin IICoculture TechniquesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyCase-Control Studiesbiology.proteinAngiotensin II Type 1 Receptor BlockersCardiovascular research
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Genetic justification of severe COVID-19 using a rigorous algorithm

2021

Recent studies suggest excessive complement activation in severe coronavirus disease-19 (COVID-19). The latter shares common characteristics with complement-mediated thrombotic microangiopathy (TMA). We hypothesized that genetic susceptibility would be evident in patients with severe COVID-19 (similar to TMA) and associated with disease severity. We analyzed genetic and clinical data from 97 patients hospitalized for COVID-19. Through targeted next-generation-sequencing we found an ADAMTS13 variant in 49 patients, along with two risk factor variants (C3, 21 patients; CFH,34 patients). 31 (32%) patients had a combination of these, which was independently associated with ICU hospitalization (…

0301 basic medicineMaleThrombomodulinSeverity of Illness Index0302 clinical medicineRisk FactorsImmunology and AllergyMedicineComplement ActivationRigorous algorithmmedicine.diagnostic_testHigh-Throughput Nucleotide SequencingComplement C3EculizumabEculizumabMiddle AgedHospitalizationSettore ICAR/09 - Tecnica Delle CostruzioniIntensive Care UnitsFactor HComplement Factor HFemaleAlgorithmsmedicine.drugmedicine.medical_specialtyThrombotic microangiopathyCritical CareImmunologyComplementADAMTS13 Protein03 medical and health sciencesInternal medicineFull Length ArticleSeverity of illnessGenetic predispositionGenetic susceptibilityHumansGenetic Predisposition to DiseaseGenetic TestingRisk factorGenetic testingAgedbusiness.industryThrombotic MicroangiopathiesCOVID-19medicine.diseaseComplement system030104 developmental biologySARS-CoV2business030215 immunologyClinical Immunology (Orlando, Fla.)
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