Search results for "Muscle Cells"

showing 10 items of 24 documents

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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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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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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Inhibition of Xanthine Oxidase by Allopurinol Prevents Skeletal Muscle Atrophy: Role of p38 MAPKinase and E3 Ubiquitin Ligases

2012

International audience; Abstract Top Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in ratsand its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinaseand the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, …

MaleAgingAnatomy and Physiology[SDV]Life Sciences [q-bio]lcsh:MedicineMuscle ProteinsGene ExpressionHindlimbSignal transductionmedicine.disease_causep38 Mitogen-Activated Protein KinasesTripartite Motif Proteinschemistry.chemical_compound0302 clinical medicineMolecular cell biologySignaling in Cellular Processeslcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarySignaling cascadesMuscle BiochemistryAnimal ModelsMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureBiochemistryHindlimb SuspensionMuscleMedicinemedicine.symptomCellular Typesmedicine.drugResearch Articlemedicine.medical_specialtyXanthine OxidaseMAPK signaling cascadesAllopurinolUbiquitin-Protein LigasesAllopurinolBiology03 medical and health sciencesAtrophyModel OrganismsInternal medicinemedicineAnimalsRats WistarXanthine oxidaseMuscle SkeletalBiology030304 developmental biologySoleus muscleMuscle CellsSKP Cullin F-Box Protein LigasesSuperoxide Dismutaselcsh:RSkeletal musclemedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryRatlcsh:QPhysiological Processes030217 neurology & neurosurgeryOxidative stress
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Exploration of lipid metabolism in relation with plasma membrane properties of Duchenne muscular dystrophy cells: influence of L-carnitine.

2012

Duchenne muscular dystrophy (DMD) arises as a consequence of mutations in the dystrophin gene. Dystrophin is a membrane-spanning protein that connects the cytoskeleton and the basal lamina. The most distinctive features of DMD are a progressive muscular dystrophy, a myofiber degeneration with fibrosis and metabolic alterations such as fatty infiltration, however, little is known on lipid metabolism changes arising in Duchenne patient cells. Our goal was to identify metabolic changes occurring in Duchenne patient cells especially in terms of L-carnitine homeostasis, fatty acid metabolism both at the mitochondrial and peroxisomal level and the consequences on the membrane structure and functi…

MaleAnatomy and PhysiologyMuscle FunctionsDuchenne muscular dystrophylcsh:MedicineDuchenne Muscular DystrophyBiochemistrychemistry.chemical_compoundPathologyMuscular dystrophylcsh:ScienceMusculoskeletal SystemPhospholipidschemistry.chemical_classificationMultidisciplinarybiologyFatty AcidsMuscle BiochemistryMitochondriaSaturated fatty acidCytochemistryMedicineMuscleDystrophinPolyunsaturated fatty acidResearch Articlemedicine.medical_specialtyAdolescentMembrane StructuresDiagnostic MedicineInternal medicineCarnitinemedicineGeneticsHumansBiologyMuscle CellsFatty acid metabolismCell Membranelcsh:RFatty acidLipid metabolismHuman GeneticsX-Linkedmedicine.diseaseLipid MetabolismMuscular Dystrophy DuchenneEndocrinologychemistrybiology.proteinlcsh:QBiomarkersMembrane CompositionGeneral PathologyPLoS ONE
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Neomyogenesis in 3D Dynamic Responsive Prosthesis for Inguinal Hernia Repair

2018

Despite undisputed improvements, prosthetics hernia repair continues to be affected by unacceptable rates of complications. Postoperative adverse events such as discomfort and chronic pain represent a subject of increasing concern among the surgical community. Poor quality biologic response, stiff scar plates, and mesh shrinkage, a typical effect of conventional static meshes and plugs, are all indicated as the main reasons for many of the complications related to inguinal hernia repair. Even the conventional concept of treatment based upon a supposed reinforcement of the groin consequent to the fibrotic incorporation of meshes, would appear to be inadequate in the light of the latest scien…

MaleMuscle CellsInguinal herniaBiomedical EngineeringTissue scaffoldMuscle CellMedicine (miscellaneous)Hernia InguinalBioengineeringMiddle AgedMuscle DevelopmentBiomaterialFollow-Up StudieProsthesis ImplantationProstheseTissue regenerationHumansMuscular tissueHerniorrhaphyFollow-Up StudiesAgedHuman
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Evidence for a role of inducible nitric oxide synthase in gastric relaxation of mdx mice

2006

Alterations of gastric mechanical activity have been reported in mdx mouse, animal model for Duchenne muscular dystrophy. This study examined if alterations in the vasoactive intestinal polypeptide (VIP) system are present in mdx stomach. Gastric mechanical activity was recorded in vitro as changes of endoluminal pressure and neurally or pharmacologically evoked relaxations were analysed in mdxvs normal stomach. Reverse-transcription polymerase chain reaction was used to detect inducible nitric oxide synthase (iNOS) expression. Relaxations to sodium nitroprusside in mdx stomach showed no difference in comparison with normal preparations. In normal stomach, VIP produced relaxation, which was…

Malemedicine.medical_specialtymdx mousePhysiologyMuscle RelaxationVasoactive intestinal peptideNitric Oxide Synthase Type IIStimulationDUCHENNES MUSCULAR-DYSTROPHYSettore BIO/09 - FisiologiaNitric oxidechemistry.chemical_compoundMiceOrgan Culture TechniquesInternal medicineQuinoxalinesmedicineAnimalsRNA MessengerEnzyme InhibitorsReceptorOxadiazolesbiologyEndocrine and Autonomic SystemsReverse Transcriptase Polymerase Chain ReactionStomachStomachGastroenterologySMOOTH-MUSCLE CELLSMuscle SmoothPEPTIDE RELEASENitric oxide synthaseMuscular Dystrophy DuchenneDisease Models AnimalEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl Esterchemistrybiology.proteinMice Inbred mdxReceptors Vasoactive Intestinal PeptideSodium nitroprussideIminesmedicine.drugVasoactive Intestinal Peptide
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FSHD muscular dystrophy region gene 1 binds Suv4-20h1 histone methyltransferase and impairs myogenesis.

2013

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant myopathy with a strong epigenetic component. It is associated with deletion of a macrosatellite repeat leading to over-expression of the nearby genes. Among them, we focused on FSHD region gene 1 (FRG1) since its over-expression in mice, Xenopus laevis and Caenorhabditis elegans, leads to muscular dystrophy-like defects, suggesting that FRG1 plays a relevant role in muscle biology. Here we show that, when over-expressed, FRG1 binds and interferes with the activity of the histone methyltransferase Suv4-20h1 both in mammals and Drosophila. Accordingly, FRG1 over-expression or Suv4-20h1 knockdown inhibits myogenesis. Moreov…

Muscle DevelopmentEvolution Molecular03 medical and health sciencesMice0302 clinical medicineGeneticsmedicineFacioscapulohumeral muscular dystrophyMyocyteAnimalsHumansEpigeneticsMuscular dystrophyMyopathyMolecular Biology030304 developmental biologyCell NucleusMice Knockout0303 health sciencesMuscle CellsbiologyMyogenesisMicrofilament ProteinsNuclear ProteinsProteinsRNA-Binding ProteinsCell DifferentiationCell BiologyGeneral MedicineHistone-Lysine N-MethyltransferaseMuscular Dystrophy Animalmedicine.diseaseMolecular biologyHistoneDrosophila melanogasterHEK293 CellsPhenotypeOrgan SpecificityHistone methyltransferaseEpigenetic deregulation by FRG1Gene Knockdown Techniquesbiology.proteinmedicine.symptomCarrier Proteins030217 neurology & neurosurgeryProtein BindingJournal of molecular cell biology
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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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De Novo prion aggregates trigger autophagy in skeletal muscle

2014

ABSTRACT In certain sporadic, familial, and infectious prion diseases, the prion protein misfolds and aggregates in skeletal muscle in addition to the brain and spinal cord. In myocytes, prion aggregates accumulate intracellularly, yet little is known about clearance pathways. Here we investigated the clearance of prion aggregates in muscle of transgenic mice that develop prion disease de novo . In addition to neurodegeneration, aged mice developed a degenerative myopathy, with scattered myocytes containing ubiquitinated, intracellular prion inclusions that were adjacent to myocytes lacking inclusions. Myocytes also showed elevated levels of the endoplasmic reticulum chaperone Grp78/BiP, su…

PrionsAutophagosome maturationanimal diseasesBlotting WesternImmunologyMice TransgenicBiologyProtein degradationPolymerase Chain ReactionMedical and Health SciencesMicrobiologyTransgenicPrion DiseasesMiceVirologyAutophagymedicineAnimalsMyocyteMuscle SkeletalEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsDNA PrimersMuscle CellsAgricultural and Veterinary SciencesBlottingEndoplasmic reticulumNeurodegenerationAutophagySkeletal muscleSkeletalBiological Sciencesmedicine.diseaseImmunohistochemistryMolecular biologynervous system diseasesmedicine.anatomical_structureInsect ScienceChaperone (protein)biology.proteinMuscleWestern
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