Search results for "Chemokine CCL2"

showing 10 items of 57 documents

CD40 ligand and MCP-1 as predictors of cardiovascular events in diabetic patients with stroke.

2009

Aim: Up-regulation of soluble CD40 ligand (sCD40L) and of monocyte chemoattractant protein-1 (MCP-1) has been found in diabetes and in patients with acute cerebral ischemia. We asked whether (i) the two molecules are similarly upregulated among non-lacunar and lacunar diabetic strokes and (ii) sCD40L and/or MCP-1 predict the risk of cardiovascular events in this setting.Methods: Ninety patients with type 2 diabetes mellitus presenting with an acute ischemic stroke (compared with 45 control subjects) were evaluated on admission and up to 36 months (median 24 months) after the event.Results: Diabetic patients with acute stroke had higher plasma CD40L and MCP-1 than controls (p<0.0001), wit…

MaleRiskCD40 ligand stroke diabetesmedicine.medical_specialtystrokeCD40L MCP-1Settore MED/09 - Medicina Internacerebral ischemia; chemokines; cytokines; diabetes mellitusCD40 LigandIschemiachemokinesDiseasecerebral ischemiaCohort StudiesDiabetes ComplicationsInternal medicineDiabetes mellitusInternal MedicineDiabetes MellitusMedicineCD40LHumanscardiovascular diseasesStrokeChemokine CCL2Ageddiabetesbusiness.industryProportional hazards modelBiochemistry (medical)Type 2 Diabetes MellitusMiddle Agedmedicine.diseasecytokinesSurgeryStrokeTreatment OutcomeQuartileGene Expression RegulationCardiologyRegression AnalysisFemaleCardiology and Cardiovascular MedicinebusinessCohort studyMCP-1
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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Incidence of Abcd1 level on the induction of cell death and organelle dysfunctions triggered by very long chain fatty acids and TNF-alpha on oligoden…

2012

X-linked adrenoleukodystrophy (X-ALD) is characterized by ABCD1 deficiency. This disease is associated with elevated concentrations of very long chain fatty acids (C24:0 and C26:0) in the plasma and tissues of patients. Under its severe form, brain demyelination and inflammation are observed. Therefore, we determined the effects of C24:0 and C26:0 on glial cells:oligodendrocytes, which synthesize myelin, and astrocytes, which participate in immune response. So, 158N murine oligodendrocytes, rat C6 glioma cells, rat primary cultures of neuronal-glial cells, and of oligodendrocytes were treated for various periods of time in the absence or presence of C24:0 and C26:0 used at plasmatic concent…

MaleTime FactorsVacuoleMitochondrionToxicologyATP Binding Cassette Transporter Subfamily D Member 1chemistry.chemical_compoundMice0302 clinical medicineRNA Small InterferingAdrenoleukodystrophyCells CulturedComputingMilieux_MISCELLANEOUSMembrane Potential MitochondrialNeurons0303 health sciencesGeneral NeuroscienceFatty AcidsBrainPeroxisomeCatalaseFlow Cytometry3. Good healthCell biologyMitochondriaOligodendrogliamedicine.anatomical_structureFemaleProgrammed cell deathChromatography GasBiologyGas Chromatography-Mass SpectrometryStatistics Nonparametric03 medical and health sciencesMicroscopy Electron TransmissionLysosomeOrganellemedicineAnimalsHumansPropidium iodideRNA MessengerRats Wistar030304 developmental biologyCell SizeChemokine CCL22OrganellesDose-Response Relationship DrugCell growthTumor Necrosis Factor-alphaRatschemistryAnimals NewbornAstrocytesATP-Binding Cassette Transporters[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: Pleiotropic evidence from plasma mRNA analyses

2013

Objective: Statin pleiotropy is still an evolving concept, and the lack of clarity on this subject is due at least in part to the lack of a definitive biomarker for statin pleiotropy. Using plasma mRNA analysis as a novel research tool for the non-invasive in vivo assessment of gene expression in vascular beds, we hypothesised that atorvastatin lowers the plasmamRNA level from statin pleiotropy-target genes, and the reduction is independent of the reduction of low-density lipoprotein cholesterol (LDL-C). Design and methods: Forty-four patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). Plasma chemokine (C-C motif) ligand 2 (CCL2) and intercellular adhesion molec…

Malemedicine.medical_specialtyChemokineStatinmedicine.drug_classAtorvastatinClinical BiochemistryGene ExpressionDrug Administration ScheduleIn vivoInternal medicineGene expressionAtorvastatinmedicineHumansPyrrolesAngina StableRNA MessengerSerum amyloid AChemokine CCL2AgedbiologyAnticholesteremic AgentsAtorvastatin CCL2 ICAM1 Interventional trial mRNA in plasma Pleiotropic effectsC-reactive proteinCholesterol LDLGeneral MedicineMiddle AgedIntercellular Adhesion Molecule-1EndocrinologyHeptanoic AcidsHMG-CoA reductasebiology.proteinFemalelipids (amino acids peptides and proteins)medicine.drugClinical Biochemistry
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Influence of HMB Supplementation and Resistance Training on Cytokine Response to Resistance Exercise

2014

The purpose of this study was to determine the effects of a multinutritional supplement including amino acids, β-hydroxy-β-methylbutyrate (HMB), and carbohydrates on cytokine responses to resistance exercise and training.Seventeen healthy, college-aged men were randomly assigned to a Muscle Armor™ (MA; Abbott Nutrition, Columbus, OH) or placebo supplement group and 12 weeks of resistance training. An acute resistance exercise protocol was administered at 0, 6, and 12 weeks of training. Venous blood samples at pre-, immediately post-, and 30-minutes postexercise were analyzed via bead multiplex immunoassay for 17 cytokines.After 12 weeks of training, the MA group exhibited decreased interfer…

Malemedicine.medical_specialtyStrength trainingmedicine.medical_treatmentInterleukin-1betaMedicine (miscellaneous)Immune functionGranulocytePlaceboBody Mass IndexInterferon-gammaYoung AdultDouble-Blind MethodMuscle damageInternal medicineMyokineMyokinemedicineDietary CarbohydratesValeratesHumansMicronutrientsAmino Acidsta315Chemokine CCL4Immune function; Muscle damage; Myokine; Nutrition; Strength trainingChemokine CCL2NutritionNutrition and DieteticsInterleukin-13business.industryInterleukin-6MonocyteBody WeightInterleukin-8InterleukinResistance TrainingVenous bloodHealthy VolunteersInterleukin-10Cytokinemedicine.anatomical_structureEndocrinologyNutrition AssessmentImmunologyDietary SupplementsCytokinesStrength trainingbusiness
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Enzymatically Degraded, Nonoxidized LDL Induces Human Vascular Smooth Muscle Cell Activation, Foam Cell Transformation, and Proliferation

2000

Background —Enzymatic, nonoxidative modification transforms LDL to an atherogenic molecule (E-LDL) that activates complement and macrophages and is present in early atherosclerotic lesions. Methods and Results —We report on the atherogenic effects of E-LDL on human vascular smooth muscle cells (SMC). E-LDL accumulated in these cells, and this was accompanied by selective induction of monocyte chemotactic protein-1 in the absence of effects on the expression of interleukin (IL)-8, RANTES, or monocyte inflammatory proteins-1α and -β). Furthermore, E-LDL stimulated the expression of gp130, the signal-transducing chain of the IL-6 receptor (IL-6R) family, and the secretion of IL-6. E-LDL invok…

Malemedicine.medical_specialtyVascular smooth muscleArteriosclerosismedicine.medical_treatmentBiologyFibroblast growth factorMuscle Smooth VascularStatistics NonparametricPhysiology (medical)Internal medicinemedicineHomeostasisHumansRNA MessengerAutocrine signallingAortaCells CulturedChemokine CCL2AgedFoam cellInterleukin-6Cell growthGrowth factorMonocyteCholesterol LDLReceptors Interleukin-6EnzymesCell biologymedicine.anatomical_structureEndocrinologyFemaleCardiology and Cardiovascular MedicineCell activationOxidation-ReductionCell DivisionFoam CellsCirculation
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The STATe of the Neuron Leads to Synaptic Stripping

2018

In a recent issue of Cell, Di Liberto et al. (2018) elucidate the mechanisms involved in synaptic stripping during viral infection. Infected neurons orchestrate their own synaptic loss downstream of IFNγ signaling, ultimately attracting phagocytic monocytes into the CNS through CCL2 production.

Neurons0301 basic medicinePhagocytesChemistryT-LymphocytesGeneral NeuroscienceCellCCL2Viral infectionMonocytes03 medical and health sciences030104 developmental biologymedicine.anatomical_structureStripping (linguistics)medicineNeuronNeuroscienceChemokine CCL2Neuron
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Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study

2013

Objectives: Traditional clinical risk factors are associated with inflammation cross-sectionally, but associations of longitudinal variation in inflammatory biomarkers with corresponding changes in clinical risk factors are incompletely described. We sought to analyze clinical factors associated with change in inflammation in the community.Methods: We studied 3013 Framingham Offspring (n = 2735) and Omni Cohort (n = 278) participants (mean age 59 years, 55% women, 9% ethnic/racial minority) who attended two consecutive examination cycles (mean 6.7 years apart). We selected ten inflammatory biomarkers representing distinctive biological functions: C-reactive protein (CRP), intercellular adhe…

OncologyMaleBLOOD-PRESSUREIsoprostanesFramingham Heart StudyRisk FactorsMyocardial infarctionOXIDATIVE STRESSskin and connective tissue diseasesChemokine CCL2Biological markersbiologyLongitudinal studiesMiddle AgedIntercellular Adhesion Molecule-1Inflammatory biomarkersC-REACTIVE PROTEINP-SelectinADIPOSE-TISSUEMassachusettsCardiovascular DiseasesCARDIOVASCULAR-DISEASEFemalemedicine.symptomCardiology and Cardiovascular MedicineVasculitisVasculitismedicine.medical_specialtyInflammationArticleInternal medicinemedicineHumansReceptors Tumor Necrosis Factor Type IIInterleukin 6AgedInflammationbusiness.industryInterleukin-6PERIPHERAL ARTERIAL-DISEASEC-reactive proteinOsteoprotegerinADHESION MOLECULE-1medicine.diseasePHOSPHOLIPASE A(2)Blood pressurePLASMA-CONCENTRATIONMYOCARDIAL-INFARCTIONImmunology1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteinsense organsbusinessBiomarkers
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Subendothelial infiltration of neutrophil granulocytes and liberation of matrix-destabilizing enzymes in an experimental model of human neo-intima.

2008

SummaryIt was the objective of this study to examine the role of human neutrophil granulocytes (PMN) in an in-vitro model of human neo-intima developed for the study of atherosclerosis. Human granulocytes were subjected to a co-culture model of human endothelial and smooth muscle cells. Subendothelial lipid accumulation was achieved by addition of native LDL to the culture medium. Tissue samples were analyzed by immunohistochemistry and scanning/transmission electron microscopy, and culture supernatants were examined for the presence of interleukin- 8 (IL-8), MCP-1, GRO-α, elastase and matrixmetalloproteinase-8 (MMP-8). Following addition of 2 mg/ml LDL, adherence, transmigration and infilt…

Pathologymedicine.medical_specialtyTime FactorsEndotheliumNeutrophilsChemokine CXCL1Myocytes Smooth MuscleApoptosisBiologyGranulocyteMuscle Smooth VascularmedicineMyocyteHumansSecretionLeukocyte RollingCells CulturedChemokine CCL2ElastaseInterleukin-8InterleukinEndothelial CellsHematologymedicine.diseaseAtherosclerosisMolecular biologyCoculture TechniquesCulture MediaExtracellular MatrixLipoproteins LDLmedicine.anatomical_structureMatrix Metalloproteinase 8Neutrophil InfiltrationApoptosisLeukocyte ElastaseTunica IntimaInfiltration (medical)Signal TransductionThrombosis and haemostasis
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