Search results for "Right ventricular hypertrophy"

showing 5 items of 5 documents

Downregulation and Nuclear Relocation of MLP During the Progression of Right Ventricular Hypertrophy Induced by Chronic Pressure Overload

2000

Abstract The cardiac LIM domain protein MLP plays a crucial role in the architecture and mechanical function of cardiac myocytes. Mice lacking the MLP gene develop cardiac hypertrophy, dilated cardiopathy and heart failure. We investigated whether downregulation of MLP is induced by pressure overload and contributes to the physiopathology of cardiac hypertrophy and failure. We studied this mechanism in rat right ventricles submitted to pulmonary arterial hypertension, because it is known that this ventricle is very vulnerable to the deleterious effects of pressure overload. During the progression of cardiac hypertrophy to failure over a 31 days period there was a dramatic decrease by 50% of…

MaleCytoplasmmedicine.medical_specialtyTime FactorsTranscription GeneticHeart VentriclesDown-RegulationMuscle ProteinsCardiomegalyCytosolMyofibrilsDownregulation and upregulationRight ventricular hypertrophyInternal medicinePressureAnimalsVentricular FunctionMedicineMyocyteRNA MessengerRats WistarLungMolecular BiologyCell NucleusHomeodomain ProteinsPressure overloadReverse Transcriptase Polymerase Chain Reactionbusiness.industryMyocardiumLIM Domain Proteinsmedicine.diseaseImmunohistochemistryPulmonary hypertensionRatsMicroscopy Electronmedicine.anatomical_structureVentricleHeart failureCardiologyCardiology and Cardiovascular MedicinebusinessMyofibrilJournal of Molecular and Cellular Cardiology
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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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Roflumilast, a phosphodiesterase 4 inhibitor, alleviates bleomycin-induced lung injury

2009

Mandarin translation of abstract Background and purpose:  The effects of a phosphodiesterase 4 (PDE4) inhibitor, roflumilast, on bleomycin-induced lung injury were explored in ‘preventive’ and ‘therapeutic’ protocols and compared with glucocorticoids. Experimental approach:  Roflumilast (1 and 5 mg·kg−1·d−1, p.o.) or dexamethasone (2.5 mg·kg−1·d−1, p.o.) was given to C57Bl/6J mice from day 1 to 14 (preventive) or day 7 to 21 (therapeutic) after intratracheal bleomycin (3.75 U·kg−1). In Wistar rats, roflumilast (1 mg·kg−1·d−1, p.o.) was compared with methylprednisolone (10 mg·kg−1·d−1, p.o.) from day 1 to 21 (preventive) or from day 10 to 21 (therapeutic), following intratracheal instillatio…

CyclopropanesMalemedicine.medical_specialtyPhosphodiesterase InhibitorsPulmonary FibrosisAminopyridinesLung injuryBiologyBleomycinBronchoalveolar Lavagechemistry.chemical_compoundBleomycinMiceFibrosisRight ventricular hypertrophyInternal medicinePulmonary fibrosismedicineAnimalsRats WistarLungDexamethasoneRoflumilastPharmacologymedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionLung Injuryrespiratory systemmedicine.diseaseResearch Papersrespiratory tract diseasesRatsMice Inbred C57BLDisease Models AnimalBronchoalveolar lavageEndocrinologychemistryBenzamidesPhosphodiesterase 4 InhibitorsBronchoalveolar Lavage Fluidmedicine.drug
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Right ventricular collagen type III and IV gene expression increases during early phases of endurance training in hypobaric hypoxic condition

1997

The objective of this study was to examine the effects of prolonged exposure to hypobaric hypoxic condition, physical training and their combination on collagen type I, III and IV gene expression in the ventricles and atria of rat heart. Male rats were assigned to four groups: normobaric sedentary (NS) and trained (NT), and hypobaric sedentary (HS) and trained (HT). Exposure to and treadmill running training in hypobaric condition were carried out in a hypobaric chamber (770–740 mbar, 2250–2550 m). Experimental periods were 10, 21 and 56 days; the groups of 91 days served as recovery groups from experimental settings of 56 days. Exposure to hypobaric condition as such and in combination wit…

MaleAtmosphere Exposure Chambersmedicine.medical_specialtyPhysiologyHeart VentriclesProcollagen-Proline DioxygenaseGene ExpressionCardiomegalyBiologyLeft ventricular hypertrophyCollagen Type IIIEndurance trainingRight ventricular hypertrophyPhysical Conditioning AnimalPhysiology (medical)Internal medicineGene expressionmedicineAnimalsHeart AtriaRNA MessengerRats WistarHypoxiaCardiac muscleBlotting Northernmedicine.diseaseRatsHydroxyprolineAtmospheric PressureEndocrinologymedicine.anatomical_structureMrna levelHypobaric chamberPhysical EnduranceCollagenCardiology and Cardiovascular MedicineBasic Research in Cardiology
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Biopterin metabolism and eNOS expression during hypoxic pulmonary hypertension in mice.

2013

International audience; Tetrahydrobiopterin (BH$_4$), which fosters the formation of and stabilizes endothelial NO synthase (eNOS) as an active dimer, tightly regulates eNOS coupling / uncoupling. Moreover, studies conducted in genetically-modified models demonstrate that BH$_4$ pulmonary deficiency is a key determinant in the pathogenesis of pulmonary hypertension. The present study thus investigates biopterin metabolism and eNOS expression, as well as the effect of sepiapterin (a precursor of BH$_4$) and eNOS gene deletion, in a mice model of hypoxic pulmonary hypertension. In lungs, chronic hypoxia increased BH$_4$ levels and eNOS expression, without modifying dihydrobiopterin (BH$_2$, t…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type III[SDV]Life Sciences [q-bio]Hypertension PulmonaryBiopterinlcsh:Medicine[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnosRight ventricular hypertrophyDihydrobiopterinInternal medicinemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsHypoxialcsh:Science[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biology0303 health sciencesMultidisciplinarybiologylcsh:RHypoxia (medical)biology.organism_classificationmedicine.diseasePulmonary hypertensionBiopterin[SDV] Life Sciences [q-bio]Disease Models AnimalTetrahydrofolate DehydrogenaseEndocrinologychemistryVentricular pressurelcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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