Search results for "Type I"

showing 10 items of 966 documents

Interleukin-1β Modulation of the Mechanobiology of Primary Human Pulmonary Fibroblasts: Potential Implications in Lung Repair

2020

Pro-inflammatory cytokines like interleukin-1&beta

Male0301 basic medicinecollagenMMP2Interleukin-1betaMicroscopy Atomic Forcelcsh:ChemistryMechanobiologyCell MovementCitoquinespulmonary fibroblastsLunglcsh:QH301-705.5Col·lagenCells CulturedSpectroscopyChemistryGeneral MedicineBiomechanical PhenomenaComputer Science ApplicationsCell biologymedicine.anatomical_structureIL-1βCollagenaseCytokinesFemaleCollagenMMPsType I collagenmedicine.drugAdultAdolescentFilamentous actinArticleCollagen Type ICatalysisInorganic ChemistryContractilityYoung Adult03 medical and health sciencesDownregulation and upregulationcell mechanicsmedicineHumansRegenerationRNA MessengerPhysical and Theoretical ChemistryFibroblastMolecular BiologyCell ProliferationWound Healing030102 biochemistry & molecular biologyOrganic ChemistryFibroblastsActinsElasticityCollagen Type I alpha 1 ChainCollagen Type III030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Cyclooxygenase 2repairInternational Journal of Molecular Sciences
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Brain BDNF levels are dependent on cerebrovascular endothelium-derived nitric oxide

2016

International audience; Scientific evidence continues to demonstrate a link between endothelial function and cognition. Besides, several studies have identified a complex interplay between nitric oxide (NO) and brain-derived neurotrophic factor (BDNF), a neurotrophin largely involved in cognition. Therefore, this study investigated the link between cerebral endothelium-derived NO and BDNF signaling. For this purpose, levels of BDNF and the phosphorylated form of endothelial NO synthase at serine 1177 (p-eNOS) were simultaneously measured in the cortex and hippocampus of rats subjected to either bilateral common carotid occlusion (n=6), physical exercise (n=6) or a combination of both (n=6) …

Male0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHippocampusPhysical exerciseTropomyosin receptor kinase BHippocampusNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemphysical exercisenitric oxideNeurotrophic factorsPhysical Conditioning AnimalInternal medicinemedicineAnimalsReceptor trkBRats WistarCerebral CortexBrain-derived neurotrophic factorbiologyChemistry[SCCO.NEUR]Cognitive science/NeuroscienceGeneral Neurosciencebrain-derived neurotrophic factorTrkB[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemRatsCerebrovascular Disorders030104 developmental biologyEndocrinologymedicine.anatomical_structurecarotid arteries occlusionnervous system[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinEndothelium VascularNeuroscience030217 neurology & neurosurgeryNeurotrophinEuropean Journal of Neuroscience
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Retinal arteriole reactivity in mice lacking the endothelial nitric oxide synthase (eNOS) gene

2018

Dysfunctional vascular endothelial nitric oxide synthase (eNOS) has been proposed to play a main pathophysiological role in various ocular diseases. The aim of the present study was to test the hypothesis that the chronic lack of eNOS impairs endothelium-dependent vasodilation in retinal arterioles. The relevance of eNOS for mediating vascular responses was studied in retinal vascular preparations from eNOS-deficient mice (eNOS-/-) and wild-type controls in vitro. Changes in luminal diameter in response to vasoactive agents were measured by videomicroscopy. The thromboxane mimetic, U46619, induced similar concentration-dependent constriction of retinal arterioles in eNOS-/- and wild-type mi…

Male0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumRetinal ArteryThromboxaneVasodilationMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineRetinal DiseasesEnosInternal medicinemedicineAnimalsEndothelial dysfunctionbiologyChemistrybiology.organism_classificationmedicine.diseaseSensory SystemsMice Inbred C57BLVasodilationNitric oxide synthaseArteriolesDisease Models AnimalOphthalmology030104 developmental biologyEndocrinologymedicine.anatomical_structureGene Expression Regulation030221 ophthalmology & optometrybiology.proteinRNACholinergicEndothelium VascularAcetylcholinemedicine.drugExperimental Eye Research
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Uncoupling of Endothelial Nitric Oxide Synthase in Perivascular Adipose Tissue of Diet-Induced Obese Mice

2015

Objective— The present study was conducted to investigate the contribution of perivascular adipose tissue (PVAT) to vascular dysfunction in a mouse model of diet-induced obesity. Approach and Results— Obesity was induced in male C57BL/6J mice with a high-fat diet for 20 weeks, and vascular function was studied with myograph. In PVAT-free aortas isolated from obese mice, the endothelium-dependent, nitric oxide–mediated vasodilator response to acetylcholine remained normal. In contrast, a clear reduction in the vasodilator response to acetylcholine was observed in aortas from obese mice when PVAT was left in place. Adipocytes in PVAT were clearly positive in endothelial nitric oxide synthase…

Male0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilator AgentsAdipose tissueAorta ThoracicVasodilation030204 cardiovascular system & hematologyArginineDiet High-FatNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdipokinesSuperoxidesEnosInternal medicineParacrine CommunicationAdipocytesmedicineAnimalsObesityEnzyme InhibitorsPhosphorylationAdiposityArginaseDose-Response Relationship DrugbiologyNitric Oxide Synthase Type IIIbiology.organism_classificationMice Inbred C57BLVasodilationArginaseDisease Models Animal030104 developmental biologyEndocrinologyAdipose TissuechemistryCytokinesInflammation MediatorsCardiology and Cardiovascular MedicineDiet-induced obeseSignal TransductionMyographArteriosclerosis, Thrombosis, and Vascular Biology
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In the rat maximal dentate activation model of partial complex epilepsy, the anticonvulsant activity of levetiracetam is modulated by nitric oxide-ac…

2009

The effects of nitric oxide-active drugs on the anticonvulsant action of the antiepileptic drug levetiracetam in an experimental model of partial complex seizures named maximal dentate gyrus activation were studied in rats. Levetiracetam was given alone or in combination with 7-nitroindazole, a preferential inhibitor of neuronal nitric oxide synthase, or with L: -arginine, the precursor of nitric oxide synthesis. The maximal dentate activation parameters were the time of latency and the durations of maximal dentate activation and afterdischarge responses. The administration of levetiracetam showed an anticonvulsant effect that was increased when given in combination with 7-nitroindazole. Th…

Male7-NitroindazoleIndazolesLevetiracetamMaximal dentate activation - Nitric oxide - Levetiracetam - Modulation - 7-Nitroindazolemedicine.medical_treatmentNitric Oxide Synthase Type IPharmacologyArginineNitric OxideSettore BIO/09 - FisiologiaNitric oxideEpilepsychemistry.chemical_compoundEpilepsy Complex PartialmedicineAnimalsDrug InteractionsEnzyme InhibitorsRats WistarMaximal dentate activation Nitric oxide Levetiracetam Modulation 7-NitroindazoleBiological PsychiatryDose-Response Relationship DrugChemistryDentate gyrusPiracetammedicine.diseaseEffective dose (pharmacology)PiracetamRatsPsychiatry and Mental healthDisease Models AnimalDrug CombinationsAnticonvulsantNeurologyDentate GyrusAnticonvulsantsNeurology (clinical)Levetiracetammedicine.drugJournal of neural transmission (Vienna, Austria : 1996)
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7-Nitroindazole blocks conditioned place preference but not hyperactivity induced by morphine.

2003

The effects of 7-nitroindazole (7-NI), a neural nitric oxide synthase (nNOS) inhibitor, on spontaneous locomotor activity, morphine-induced hyperactivity, acquisition of place conditioning and morphine-induced conditioned place preference (CPP) were evaluated in male mice. In experiment 1, animals treated with 7-NI (25, 50 and 100 mg/kg), morphine (40 mg/kg) or morphine (40 mg/kg) plus 7-NI (25, 50 or 100 mg/kg) were placed in an actimeter for 3 h. In experiment 2, animals treated with the same drugs and doses were conditioned following an unbiased procedure. 7-NI did not affect the spontaneous locomotor activity or hyperactivity induced by morphine. However, the moderate and high doses of …

Male7-NitroindazoleIndazolesRatónMale miceNitric Oxide Synthase Type IPharmacologyHyperkinesisMotor ActivityNitric oxideDevelopmental psychologyBehavioral Neurosciencechemistry.chemical_compoundMiceRewardmedicineAnimalsEnzyme InhibitorsbiologyDose-Response Relationship DrugMorphineConditioned place preferenceNitric oxide synthaseAnalgesics OpioidchemistryMorphinebiology.proteinConditioningConditioning OperantNitric Oxide Synthasemedicine.drugBehavioural brain research
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Treatment with soluble activin type IIB-receptor improves bone mass and strength in a mouse model of Duchenne muscular dystrophy.

2016

Background Inhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength. Duchenne muscular dystrophy (DMD) is a neuromuscular disorder that leads to progressive muscle degeneration and also high incidence of fractures. The aim of our study was to test whether inhibition of activin receptor IIB ligands with or without exercise could improve bone strength in the mdx mouse model for DMD. Methods Thirty-two mdx mice were divided to running and non-running groups and to receive either PBS control or soluble activin type IIB-receptor (ActRIIB-Fc) once weekly for 7 weeks. Results Treatment of mdx mice with ActRIIB-Fc resulted in significantly in…

MaleActivin Receptors Type IIDrug Evaluation PreclinicalOsteoclastsBone μCTBone and BonesMiceTGF-βsBone DensityPhysical Conditioning AnimalAnimalsBone ResorptionMuscle SkeletalExerciseOsteoblastsOrgan SizeMuscular Dystrophy AnimalCombined Modality TherapyBone-muscle interactionsAnimal modelsMice Inbred C57BLMuscular Dystrophy DuchenneDisease Models AnimalSolubilityMice Inbred mdxResearch ArticleBMC musculoskeletal disorders
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Inhibitory responses to exogenous adenosine in murine proximal and distal colon”

2006

The aims of the present study were firstly, to characterize pharmacologically the subtypes of P(1) purinoreceptors involved in the inhibitory effects induced by exogenous adenosine in longitudinal smooth muscle of mouse colon, and secondly, to examine differences in the function and distribution of these receptors between proximal and distal colon. Adenosine (100 microM-3 mM) caused a concentration-dependent reduction of the amplitude of spontaneous contractions in the proximal colon, and muscular relaxation in the distal colon. In the proximal colon, adenosine effects were antagonized by a selective A(1) receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 nM), but were not m…

MaleAdenosineNitric Oxide Synthase Type IIIColonmouse colonadenosine A2B receptorNitric OxideSettore BIO/09 - FisiologiaMiceP1 purinoreceptorAnimalsadenosine A3 receptorEnzyme InhibitorsDose-Response Relationship Drugadenosine A1 receptorReceptors Purinergic P1Muscle SmoothTriazolesnitrergic nervesMice Inbred C57BLNG-Nitroarginine Methyl Esteradenosine A2 receptorPurinergic P1 Receptor AntagonistsXanthinesPapersQuinazolinesTheobrominemechanical activityMuscle ContractionSignal Transduction
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Identification of Novel pro-α2(IX) Collagen Gene Mutations in Two Families with Distinctive Oligo-Epiphyseal Forms of Multiple Epiphyseal Dysplasia

1999

Multiple epiphyseal dysplasia (MED) is a genetically heterogeneous disorder with marked clinical and radiographic variability. Traditionally, the mild "Ribbing" and severe "Fairbank" types have been used to define a broad phenotypic spectrum. Mutations in the gene encoding cartilage oligomeric-matrix protein have been shown to result in several types of MED, whereas mutations in the gene encoding the alpha2 chain of type IX collagen (COL9A2) have so far been found only in two families with the Fairbank type of MED. Type IX collagen is a heterotrimer of pro-alpha chains derived from three distinct genes-COL9A1, COL9A2, and COL9A3. In this article, we describe two families with distinctive ol…

MaleAdolescentRNA SplicingMutantGene mutationBiologyOsteochondrodysplasiasmedicine.disease_causeMultiple epiphyseal dysplasia03 medical and health sciencesExon0302 clinical medicineOsteoarthritismedicineGeneticsHumansGenetics(clinical)Genetic TestingOsteochondrodysplasiaMultiple epiphyseal dysplasiaGene mutationAlleleChildPolymorphism Single-Stranded ConformationalGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationType IX collagenGenetic heterogeneitymedicine.diseaseOsteochondrodysplasiaPedigreeRadiographyCartilageChild PreschoolMutationFemaleEpiphysesProcollagen030217 neurology & neurosurgeryResearch ArticleThe American Journal of Human Genetics
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