Search results for "Vascular Remodeling"

showing 10 items of 20 documents

Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular,…

0301 basic medicineJanus kinase 2 (JAK2)QH301-705.5Hypertension PulmonaryInflammationReviewVascular Remodeling030204 cardiovascular system & hematologyModels BiologicalCatalysisstatInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicine.arterymedicineAnimalsHumanssignal transducer and activator of transcription 3 (STAT3)pulmonary hypertension (PH)Physical and Theoretical ChemistryEndothelial dysfunctionBiology (General)Molecular BiologyQD1-999SpectroscopyJanus Kinasesbiologybusiness.industryOrganic ChemistryJAK-STAT signaling pathwayGeneral Medicinemedicine.diseasePulmonary hypertensionComputer Science ApplicationsSTAT Transcription FactorsChemistry030104 developmental biologyPulmonary arterybiology.proteinCancer researchmedicine.symptombusinessMyofibroblastPlatelet-derived growth factor receptorSignal TransductionInternational Journal of Molecular Sciences
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The Role of Sirtuin1 in Regulating Endothelial Function, Arterial Remodeling and Vascular Aging

2019

Sirtuin1 (SIRT1), which belongs to a highly conserved family of protein deacetylase, is one of the best-studied sirtuins. SIRT1 is involved in a variety of biological processes, including energy metabolism, cell proliferation and survival, chromatin dynamics, and DNA repair. In the vasculature, SIRT1 is ubiquitously expressed in endothelial cells, smooth muscle cells, and perivascular adipose tissues (PVAT). Endothelial SIRT1 plays a unique role in vasoprotection by regulating a large variety of proteins, including endothelial nitric oxide synthase (eNOS). In endothelial cells, SIRT1 and eNOS regulate each other synergistically through positive feedback mechanisms for the maintenance of end…

0301 basic medicinePhysiologyDNA repairvascular remodelingAdipose tissueReview030204 cardiovascular system & hematologylcsh:Physiology03 medical and health sciencesSIRT10302 clinical medicineEnosPhysiology (medical)lcsh:QP1-981biologyCell growthbiology.organism_classificationChromatinCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologyvascular agingPVATeNOSProtein deacetylaseVascular aginghormones hormone substitutes and hormone antagonistsFunction (biology)Frontiers in Physiology
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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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Resveratrol and the Interaction between Gut Microbiota and Arterial Remodelling

2020

Arterial remodelling refers to the alteration in the structure of blood vessel that contributes to the progression of hypertension and other cardiovascular complications. Arterial remodelling is orchestrated by the crosstalk between the endothelium and vascular smooth muscle cells (VSMC). Vascular inflammation participates in arterial remodelling. Resveratrol is a natural polyphenol that possesses anti-oxidant and anti-inflammatory properties and has beneficial effects in both the endothelium and VSMC. Resveratrol has been studied for the protective effects in arterial remodelling and gut microbiota, respectively. Gut microbiota plays a critical role in the immune system and inflammatory pr…

0301 basic medicineVascular smooth muscleEndotheliumMyocytes Smooth MusclePopulationlcsh:TX341-641InflammationReviewresveratrolVascular Remodeling030204 cardiovascular system & hematologyResveratrolGut floraPharmacologydigestive systemAntioxidantsMuscle Smooth VascularVascular remodelling in the embryo03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumanseducationCell ProliferationNeointimal hyperplasiaeducation.field_of_studyNutrition and Dieteticsgut microbiotabiologybusiness.industryanti-oxidantSIRT1 arterial remodellingArteriesmedicine.diseasebiology.organism_classificationGastrointestinal Microbiome030104 developmental biologymedicine.anatomical_structurechemistryinflammationcardiovascular systemmedicine.symptombusinesslcsh:Nutrition. Foods and food supplyFood ScienceNutrients
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Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
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Phosphodiesterase-5 Inhibition Alleviates Pulmonary Hypertension and Basal Lamina Thickening in Rats Challenged by Chronic Hypoxia

2018

javax.xml.bind.JAXBElement@6f8948ff Hypoxia represents both an outcome of cardiopulmonary diseases and a trigger for severe pulmonary complications as pulmonary hypertension. Because nitric oxide (NO) is a critical mediator in the development of pulmonary hypertension, the modulators of its downstream function may become target of pharmacological interventions aimed at alleviating the impact of this condition. Here, we investigate the effects of an early administration of phosphodiesterase-5 inhibitor in rats where pulmonary artery hypertension was induced by chronic exposure to hypoxia. javax.xml.bind.JAXBElement@162dc677 Rats were divided into three groups: normoxic control, hypoxic with …

0301 basic medicinemedicine.medical_specialtynitrites and nitratesPhysiologySildenafilsildenafil030204 cardiovascular system & hematologyphosphodiesterase 5lcsh:PhysiologyNitric oxideendothelial NO synthase; nitric oxide; nitrites and nitrates; phosphodiesterase 5; pulmonary hypertension; pulmonary vascular remodeling; right heart failure; sildenafil03 medical and health scienceschemistry.chemical_compound0302 clinical medicinenitric oxidePhysiology (medical)medicine.arteryInternal medicinepulmonary hypertensionmedicineendothelial NO synthaseOriginal ResearchCardiopulmonary diseaseLunglcsh:QP1-981business.industryright heart failureHypoxia (medical)medicine.diseasePulmonary hypertension030104 developmental biologymedicine.anatomical_structurechemistryVentriclePulmonary arteryCardiologymedicine.symptombusinesspulmonary vascular remodelingFrontiers in Physiology
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Shear Stress and Aortic Strain Associations With Biomarkers of Ascending Thoracic Aortic Aneurysm

2019

This study aims to investigate the association of wall shear stress (WSS) and aortic strain with circulating biomarkers including matrix metalloproteinases (MMP), tissue inhibitors of metalloproteinase (TIMP), and exosomal level of microRNA (miRNA) in ascending aortic aneurysms of patients with bicuspid or tricuspid aortic valve.A total of 76 variables from 125 patients with ascending aortic aneurysms were collected from (1) blood plasma to measure plasma levels of miRNAs and protein activity; (2) computational flow analysis to estimate peak systolic WSS and time-average WSS (TAWSS); and (3) imaging analysis of computed tomography angiography to determine aortic wall strain. Principal compo…

AdultMalePulmonary and Respiratory MedicineAortic valvemedicine.medical_specialtybicuspid aortic valveVascular Remodeling030204 cardiovascular system & hematologyMechanotransduction CellularThoracic aortic aneurysm03 medical and health sciencesAortic aneurysm0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve Diseaseascending thoracic aortic aneurysmMatrix Metalloproteinase 12medicine.arteryInternal medicineAscending aortamedicineHumansAortaAgedComputed tomography angiographyAortaTissue Inhibitor of Metalloproteinase-1Aortic Aneurysm Thoracicmedicine.diagnostic_testbusiness.industrybiomarkersSettore ING-IND/34 - Bioingegneria IndustrialeMiddle Agedmedicine.diseaseMicroRNAsLogistic ModelsBlood pressuremedicine.anatomical_structure030228 respiratory systemAortic Valvecardiovascular systemCardiologyFemaleSurgeryStress MechanicalMatrix Metalloproteinase 1Cardiology and Cardiovascular MedicinebusinessThe Annals of Thoracic Surgery
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Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

2016

Background Ascending thoracic aortic aneurysm ( ATAA ) is driven by angiotensin II (Ang II ) and contributes to the development of left ventricular ( LV ) remodeling through aortoventricular coupling. We previously showed that locally available leptin augments Ang II ‐induced abdominal aortic aneurysms in apolipoprotein E–deficient mice. We hypothesized that locally synthesized leptin mediates Ang II ‐induced ATAA . Methods and Results Following demonstration of leptin synthesis in samples of human ATAA associated with different etiologies, we modeled in situ leptin expression in apolipoprotein E–deficient mice by applying exogenous leptin on the surface of the ascending aorta. This treatm…

LeptinMale0301 basic medicineAortic valveTranslational StudiesMice Knockout ApoEaortic valve stenosisangiotensin II030204 cardiovascular system & hematologyLeft ventricular hypertrophyVascular MedicineMiceAortic aneurysm0302 clinical medicineVasoconstrictor AgentsMedicineCells CulturedOriginal ResearchAged 80 and overVentricular RemodelingLeptindigestive oral and skin physiologyMiddle Agedleft ventricular hypertrophymedicine.anatomical_structureAortic ValveAortic valve stenosiscardiovascular systemCardiologyFemaleHypertrophy Left VentricularCardiology and Cardiovascular Medicineaortic aneurysmhormones hormone substitutes and hormone antagonistsAdultmedicine.medical_specialtyvascular remodelingThoracic aortic aneurysmYoung Adult03 medical and health sciencesVascular Stiffnessmedicine.arteryInternal medicineAscending aortaAnimalsHumansAgedCell ProliferationAortic Aneurysm Thoracicbusiness.industryleptin antagonistmedicine.diseaseAneurysmAngiotensin II030104 developmental biologyEndocrinologyAnimal Models of Human DiseaseValvular Heart DiseasebusinessJournal of the American Heart Association
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Chronic Administration of Quercetin Induces Biomechanical and Pharmacological Remodeling in the Rat Coronary Arteries

2017

Acute dilation brought about by the dietary flavonoid quercetin in coronary arterioles has been described earlier, but no information is available on its chronic effects. Male Wistar rats (body weight about 190 g) were divided to two groups: the quercetin-treated group (n=22) had quercetin supplementation of approximately 30 mg/kg/day, whereas the control group (n=20) had none. After eight weeks of treatment, intramural coronary arterioles with identical passive diameters (178+/-14 microm and 171+/-9 microm) were prepared and their biomechanics and pharmacological reactivities were tested using pressure arteriography ex vivo. The spontaneous tone of quercetin-treated arteries was higher (16…

Male0301 basic medicinemedicine.medical_specialtyPhysiologyVasodilator AgentsLumen (anatomy)Vascular Remodeling030204 cardiovascular system & hematologyBody weightDrug Administration ScheduleNitric oxide03 medical and health scienceschemistry.chemical_compoundCoronary circulation0302 clinical medicineInternal medicinemedicineAnimalsRats WistarNo releaseGeneral MedicineCoronary VesselsRatsVasodilationCoronary arteries030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistryQuercetinQuercetinEx vivoPhysiological Research
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