Search results for "Smooth muscle cells"

showing 9 items of 9 documents

Type 5 phosphodiesterase (PDE5) and the vascular tree: from embryogenesis to aging and disease

2020

Highlights • Vascular development depends on the timely differentiation of endothelial and smooth muscle cells, that mutually influence their developmental fate. • Endothelial and vascular smooth muscle cell (VSMC) compartments can mutually influence cell and tissue modifications during vascular aging and in vascular disease. • Keeping in mind that PDE5 is mainly expressed in VSMCs, we surveyed the literature on the role of PDE5 in vascular development, aging and disease. • Although most results have been obtained by PDE5 pharmacological inhibition, no data are available, to date, on vascular development, aging or disease following PDE5 genetic ablation.

0301 basic medicineCell typeAgingVascular smooth muscleMyocytes Smooth MuscleVSMCsEmbryonic DevelopmentECsContext (language use)DiseaseBiologyMuscle Smooth VascularArticle03 medical and health sciences0302 clinical medicinenitric oxidevascular smooth muscle cellsHumansBioresorbable vascular scaffoldCyclic Nucleotide Phosphodiesterases Type 5ECEmbryogenesisPhosphodiesteraseVascular agingCell biologycGMPSettore MED/23ECs; PDE5; VSMCs; cGMP; nitric oxide030104 developmental biologyVascular aging; vascular smooth muscle cells; phosphodiesterasePDE5phosphodiesterase030217 neurology & neurosurgeryFunction (biology)Developmental Biology
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Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib

2020

Background: Carfilzomib&rsquo

Male0301 basic medicinevasculature030204 cardiovascular system & hematologyPharmacologyDinoprostEndoplasmic Reticulumlcsh:ChemistryMicechemistry.chemical_compound0302 clinical medicineAMP-Activated Protein Kinase Kinasesvascular smooth muscle cellsCytotoxicitylcsh:QH301-705.5endoplasmatic-reticulum stressSpectroscopychemistry.chemical_classificationcarfilzomibCobaltGeneral MedicineMetforminComputer Science ApplicationsRespiratory burstMetforminDrug Therapy CombinationGlycolysisOligopeptidesProteasome Inhibitorsmedicine.drugProteasome Endopeptidase ComplexautophagyCell SurvivalMyocytes Smooth MuscleAntineoplastic AgentsNitric OxideArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyReactive oxygen speciesbusiness.industryOrganic ChemistryAutophagyCarfilzomibActinsVasoprotectiveMice Inbred C57BLGlucose030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Proteasome inhibitorTumor Suppressor Protein p53Reactive Oxygen SpeciesbusinessProtein KinasesInternational Journal of Molecular Sciences
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JAK2 mediates lung fibrosis, pulmonary vascular remodelling and hypertension in idiopathic pulmonary fibrosis: an experimental study

2018

BackgroundPulmonary hypertension (PH) is a common disorder in patients with idiopathic pulmonary fibrosis (IPF) and portends a poor prognosis. Recent studies using vasodilators approved for PH have failed in improving IPF mainly due to ventilation (V)/perfusion (Q) mismatching and oxygen desaturation. Janus kinase type 2 (JAK2) is a non-receptor tyrosine kinase activated by a broad spectrum of profibrotic and vasoactive mediators, but its role in PH associated to PH is unknown.ObjectiveThe study of JAK2 as potential target to treat PH in IPF.Methods and resultsJAK2 expression was increased in pulmonary arteries (PAs) from IPF (n=10; 1.93-fold; P=0.0011) and IPF+PH (n=9; 2.65-fold; P<0.00…

0301 basic medicinePulmonary and Respiratory Medicinemedicine.medical_specialtyHypertension PulmonaryBlotting WesternMyocytes Smooth MuscleFluorescent Antibody TechniqueVasodilationVascular RemodelingReal-Time Polymerase Chain ReactionVascular remodelling in the embryo03 medical and health sciencesIdiopathic pulmonary fibrosisTransforming Growth Factor betaRight ventricular hypertrophyInternal medicinepulmonary hypertensionAnimalsHumansMedicineRNA Small InterferingRats WistarCells CulturedCell ProliferationBKCaJanus kinase 2biologybusiness.industryEndothelial CellsJanus Kinase 2idiopathic pulmonary fibrosismedicine.diseaseImmunohistochemistryPulmonary hypertensionIdiopathic Pulmonary FibrosisTriterpenesRatsPhenotype030104 developmental biologyJAK2biology.proteinCardiologyAnimal studiesJanus kinasebusinessSignal TransductionPulmonary artery smooth muscle cells Pulmonary artery endothelial cells.Thorax
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CO-releasing binuclear rhodium complexes as inhibitors of nitric oxide generation in stimulated macrophages.

2013

Nontoxic CO-releasing dirhodium complexes act as inhibitors of NO in stimulated macrophage cells, suggesting that novel antiinflammatory treatments could involve the use of these types of binuclear complexes.

StereochemistryAnti-Inflammatory Agentschemistry.chemical_elementApoptosisNitric OxideModels BiologicalNitric oxideRhodiumCell LineInorganic Chemistrychemistry.chemical_compoundQUIMICA ORGANICACoordination ComplexesQUIMICA ANALITICAMacrophageMoleculeAnimalsHumansRhodiumPhysical and Theoretical ChemistryCarbon monoxideCarbon MonoxideMacrophagesRegulatorQUIMICA INORGANICAMoleculesHeme oxygenaseHeme oxygenaseCormschemistrySmooth muscle cellsCell cultureApoptosisBiological AssayCarbon monoxideInorganic chemistry
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Elevated levels of 2-arachidonoylglycerol promote atherogenesis in ApoE-/- mice.

2018

Background The endocannabinoid (eCB) 2-arachidonoylglycerol (2-AG) is a known modulator of inflammation and ligand to both, pro-inflammatory cannabinoid receptor 1 (CB1) and anti-inflammatory CB2. While the role of both receptors in atherogenesis has been studied extensively, the significance of 2-AG for atherogenesis is less well characterized. Methods The impact of 2-AG on atherogenesis was studied in two treatment groups of ApoE-/- mice. One group received the monoacylglycerol lipase (MAGL)-inhibitor JZL184 [5 mg/kg i.p.], which impairs 2-AG degradation and thus causes elevated 2-AG levels, the other group received vehicle for four weeks. Simultaneously, both groups were fed a high-chole…

Male0301 basic medicineCCR1Chemokinelcsh:MedicineSmooth Muscle Cells030204 cardiovascular system & hematologyPathology and Laboratory MedicineBiochemistryMonocytesWhite Blood CellsMicechemistry.chemical_compoundChemokine receptorSpectrum Analysis Techniques0302 clinical medicinePiperidinesAnimal CellsCell MovementMedicine and Health SciencesReceptorlcsh:ScienceImmune ResponseJZL184MultidisciplinarybiologyNeurochemistryFlow CytometryLipidsCholesterolSpectrophotometryCytophotometryCellular TypesNeurochemicalsAnatomymedicine.symptomResearch Articlemedicine.medical_specialtyImmune CellsImmunologyMuscle TissueAntigens Differentiation MyelomonocyticInflammationArachidonic AcidsResearch and Analysis MethodsDiet High-FatCell LineGlycerides03 medical and health sciencesSigns and SymptomsApolipoproteins EDiagnostic MedicineAntigens CDInternal medicinemedicineAnimalsOil Red OBenzodioxolesInflammationMuscle CellsBlood CellsMacrophageslcsh:RBiology and Life SciencesCell BiologyAtherosclerosisMonoacylglycerol lipaseBiological Tissue030104 developmental biologyEndocrinologychemistrybiology.proteinlcsh:QEndocannabinoidsNeurosciencePLoS ONE
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Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14)

2021

Abdominal aortic aneurysm (AAA), is a complex disorder characterized by vascular vessel wall remodeling. LIGHT (TNFSF14) is a proinflammatory cytokine associated with vascular disease. In the present study, the impact of genetic inactivation of Light was investigated in dissecting AAA induced by angiotensin II (AngII) in the Apolipoprotein E-deficient (Apoe−/−) mice. Studies in aortic human (ah) vascular smooth muscle cells (VSMC) to study potential translation to human pathology were also performed. AngII-treated Apoe−/−Light−/− mice displayed increased abdominal aorta maximum diameter and AAA severity compared with Apoe−/− mice. Notably, reduced smooth muscle α-actin+ area and Acta2 and C…

Dissecting Abdominal Aortic Aneurysmmedicine.medical_specialtyVascular smooth musclebiologyApolipoprotein BQH301-705.5ChemistryMedicine (miscellaneous)Angiotensin IIArticleTNFSF14/LIGHTGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineabdominal aortic aneurysmEndocrinologyLymphotoxinInternal medicinecardiovascular systembiology.proteinmedicinevascular smooth muscle cellsGene silencingBiology (General)ACTA2Biomedicines
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Germ-free housing conditions do not affect aortic root and aortic arch lesion size of late atherosclerotic low-density lipoprotein receptor-deficient…

2020

The microbiota has been linked to the development of atherosclerosis, but the functional impact of these resident bacteria on the lesion size and cellular composition of atherosclerotic plaques in the aorta has never been experimentally addressed with the germ-free low-density lipoprotein receptor-deficient (Ldlr(-/-)) mouse atherosclerosis model. Here, we report that 16 weeks of high-fat diet (HFD) feeding of hypercholesterolemicLdlr(-/-)mice at germ-free (GF) housing conditions did not impact relative aortic root plaque size, macrophage content, and necrotic core area. Likewise, we did not find changes in the relative aortic arch lesion size. However, late atherosclerotic GFLdlr(-/-)mice …

0301 basic medicineAortic archMalePathologyaortic rootAortic rootaortic archFunctional impactAorta ThoracicHYPERCHOLESTEROLEMIAMice0302 clinical medicineDeficient mouse610 Medicine & healthMice KnockoutBILE-ACIDSCellular compositionMicrobiotaCHOLESTEROLGUT MICROBIOTAGastroenterologyinflammatory markersHousing AnimalPlaque Atheroscleroticmacrophagessmooth muscle cellsInfectious Diseasesgerm-free030211 gastroenterology & hepatologyFemalelipids (amino acids peptides and proteins)SEXTRIMETHYLAMINEmedicine.symptomMicrobiology (medical)medicine.medical_specialty610 Medicine & healthBiologyMETABOLISMlesion sizeMicrobiologyLesion03 medical and health sciencesINFLAMMATIONmedicine.arterymedicineAnimalsGerm-Free LifeHumanslcsh:RC799-869AddendumMice Inbred C57BLDisease Models Animal030104 developmental biologyReceptors LDLlow-density lipoprotein receptor-deficient mouseageLDL receptorlcsh:Diseases of the digestive system. Gastroenterologyatherosclerosis
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PCSK9 Confers Inflammatory Properties to Extracellular Vesicles Released by Vascular Smooth Muscle Cells

2022

Vascular smooth muscle cells (VSMCs) are key participants in both early- and late-stage atherosclerosis and influence neighbouring cells possibly by means of bioactive molecules, some of which are packed into extracellular vesicles (EVs). Proprotein convertase subtilisin/kexin type 9 (PCSK9) is expressed and secreted by VSMCs. This study aimed to unravel the role of PCSK9 on VSMCs-derived EVs in terms of content and functionality. EVs were isolated from human VSMCs overexpressing human PCSK9 (VSMCPCSK9-EVs) and tested on endothelial cells, monocytes, macrophages and in a model of zebrafish embryos. Compared to EVs released from wild-type VSMCs, VSMCPCSK9-EVs caused a rise in the expression …

Myocytes Smooth MusclePCSK9; atherosclerosis; extracellular vesicles; inflammation; vascular smooth muscle cellsPCSK9; atherosclerosis; extracellular vesicles; inflammation; vascular smooth muscle cells.Muscle Smooth VascularCatalysisPCSK9Inorganic ChemistryExtracellular VesiclesSettore BIO/13 - Biologia ApplicataSettore MED/44 - Medicina del Lavorovascular smooth muscle cellsAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyZebrafishSpectroscopySettore MED/04 - Patologia GeneraleOrganic ChemistryEndothelial CellsGeneral MedicineComputer Science Applicationsinflammationextracellular vesicles; PCSK9; atherosclerosis; inflammation; vascular smooth muscle cellsSettore BIO/14 - FarmacologiaatherosclerosisProprotein Convertase 9International Journal of Molecular Sciences
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Artichoke, Cynarin and Cyanidin Downregulate the Expression of Inducible Nitric Oxide Synthase in Human Coronary Smooth Muscle Cells

2014

Artichoke (Cynara scolymus L.) is one of the world’s oldest medicinal plants with multiple health benefits. We have previously shown that artichoke leaf extracts and artichoke flavonoids upregulate the gene expression of endothelial-type nitric oxide synthase (eNOS) in human endothelial cells. Whereas NO produced by the eNOS is a vasoprotective molecule, NO derived from the inducible iNOS plays a pro-inflammatory role in the vasculature. The present study was aimed to investigate the effects of artichoke on iNOS expression in human coronary artery smooth muscle cells (HCASMC). Incubation of HCASMC with a cytokine mixture led to an induction of iNOS mRNA expression. This iNOS induction was c…

Cynara scolymus L.nitric oxide; inducible NO synthase; vascular smooth muscle cells; artichoke; <i>Cynara scolymus</i> L.Myocytes Smooth MuscleCyanidinDown-RegulationNitric Oxide Synthase Type IIPharmaceutical ScienceCynarosidePharmacologyMuscle Smooth VascularArticleAnalytical ChemistryNitric oxideAnthocyaninslcsh:QD241-441chemistry.chemical_compoundlcsh:Organic chemistryEnosnitric oxideCynara scolymusDrug DiscoveryGene expressionHumansvascular smooth muscle cellsPhysical and Theoretical ChemistryPromoter Regions GeneticCells CulturedbiologyPlant Extractsinducible NO synthaseOrganic Chemistrybiology.organism_classificationCoronary VesselsVasoprotectivePlant LeavesNitric oxide synthaseGene Expression RegulationchemistryBiochemistryCinnamatesChemistry (miscellaneous)biology.proteinMolecular MedicineLuteolinartichokeMolecules
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