Search results for "Myosin Heavy Chain"

showing 10 items of 19 documents

Sex-based differences after a single bout of exercise on PGC1α isoforms in skeletal muscle: A pilot study

2020

To date, there are limited and incomplete data on possible sex-based differences in fiber-types of skeletal muscle and their response to physical exercise. Adult healthy male and female mice completed a single bout of endurance exercise to examine the sex-based differences of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), heat shock protein 60 (Hsp60), interleukin 6 (IL-6) expression, as well as the Myosin Heavy Chain (MHC) fiber-type distribution in soleus and extensor digitorum longus (EDL) muscles. Our results showed for the first time that in male soleus, a muscle rich of type IIa fibers, endurance exercise activates specifically genes involved in mito…

0301 basic medicineMalemedicine.medical_specialtyAlpha (ethology)interleukin 6Physical exerciseMotor ActivityBiochemistryMitochondrial Proteins03 medical and health sciencesMice0302 clinical medicineSex FactorsEndurance trainingphysical exerciseInternal medicineHeat shock proteinMyosinGeneticsmedicineAnimalsProtein Isoformsskeletal muscleInterleukin 6Muscle SkeletalMolecular BiologyMice Inbred BALB Cbiologybusiness.industryInterleukin-6Myosin Heavy ChainSkeletal muscleChaperonin 60musculoskeletal systemPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisbiology.proteinFemalebusiness030217 neurology & neurosurgeryheat shock protein 60Biotechnology
researchProduct

Role of skeletal muscle-fibre type in regulation of glucose metabolism in middle-aged subjects with impaired glucose tolerance during a long-term exe…

2005

Aim: The aim of this study was to investigate the role of skeletal muscle fibre type in the regulation of glucose metabolism in middle-aged obese subjects with impaired glucose tolerance (IGT) during a 2-year exercise anddietary intervention. Methods: Muscle biopsies (musculus vastus lateralis) were taken from 22 subjects belonging to the intervention group of the Finnish Diabetes Prevention Study [1]. According to their myosin heavy chain (MHC) profile at the baseline, the subjects were divided into two groups: IGT s l o w (n = 10) with a high proportion of MHC I isoforms and IGT f a s t (n = 12) with a high proportion of MHC II isoforms in the vastus lateralis muscle. The intervention con…

AdultBlood GlucoseMaleVascular Endothelial Growth Factor Amedicine.medical_specialtyDiet Reducingendocrine system diseasesVastus lateralis muscleEndocrinology Diabetes and MetabolismMuscle Fibers SkeletalCarbohydrate metabolismImpaired glucose toleranceGlycogen Synthase Kinase 3EndocrinologyInsulin resistanceDiabetes mellitusInternal medicineGlucose IntoleranceWeight LossInternal MedicinemedicineHumansAerobic exerciseObesityMuscle SkeletalGlycogen synthaseExerciseAgedMyosin Heavy Chainsbiologybusiness.industrynutritional and metabolic diseasesSkeletal muscleMiddle Agedmedicine.diseaseCombined Modality Therapymedicine.anatomical_structureEndocrinologybiology.proteinFemalebusinesshormones hormone substitutes and hormone antagonistsFollow-Up StudiesDiabetes, Obesity and Metabolism
researchProduct

Mutations in myosin heavy chain 11 cause a syndrome associating thoracic aortic aneurysm/aortic dissection and patent ductus arteriosus

2006

We have recently described two kindreds presenting thoracic aortic aneurysm and/or aortic dissection ( TAAD) and patent ductus arteriosus (PDA)(1,2) and mapped the disease locus to 16p12.2-p13.13 (ref. 3). We now demonstrate that the disease is caused by mutations in the MYH11 gene affecting the C-terminal coiled-coil region of the smooth muscle myosin heavy chain, a specific contractile protein of smooth muscle cells (SMC). All individuals bearing the heterozygous mutations, even if asymptomatic, showed marked aortic stiffness. Examination of pathological aortas showed large areas of medial degeneration with very low SMC content. Abnormal immunological recognition of SM-MHC and the colocal…

AdultMalePathologymedicine.medical_specialty[SDV]Life Sciences [q-bio]Molecular Sequence DataANEURYSM/DISSECTION030204 cardiovascular system & hematologyBiologyThoracic aortic aneurysmProtein Structure SecondaryDISEASEFamilial thoracic aortic aneurysmCOILED-COILS03 medical and health sciencesAortic aneurysm0302 clinical medicineDuctus arteriosusGeneticsmedicineMYH11LOCUSHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceDuctus Arteriosus Patent[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyAortic dissection0303 health sciencesAortic Aneurysm ThoracicBase SequenceMyosin Heavy ChainsSMC proteinHEAVY-CHAIN ISOFORMSAnatomymedicine.diseasePedigreeAortic Dissectionmedicine.anatomical_structureMutationbiology.proteincardiovascular systemFemaleACTA2SMOOTH-MUSCLE MYOSIN
researchProduct

Immunohistochemical characterization of endometriosis-associated smooth muscle cells in human peritoneal endometriotic lesions

2011

Background Smooth muscle cells (SMC) are common components of endometriotic lesions. SMC have been characterized previously in peritoneal, ovarian and deep infiltrating endometriotic lesions and adenomyosis. The aim of this retrospective study was to investigate the extent of differentiation in endometriosis-associated SMC (EMaSMC) in peritoneal endometriotic lesions. Methods We obtained biopsies from peritoneal endometriotic lesions (n = 60) and peritoneal sites distant from the endometriotic lesion (n = 60), as well as healthy peritoneum from patients without endometriosis (control tissue, n = 10). These controls were hysterectomy specimens from patients without endometriosis or adenomyos…

AdultendometriosisPathologymedicine.medical_specialtyBiopsyEndometriosisEstrogen receptorsmooth muscle metaplasiaPeritoneumRetrospective StudieProgesterone receptormedicinevasopressin receptorHumansMyocyteAdenomyosisEndometriosiOxytocin receptorRetrospective Studiesendometriosis; Oxytocin receptor; smooth muscle metaplasiaMyosin Heavy Chainsbusiness.industryRehabilitationMyosin Heavy ChainObstetrics and GynecologyCell DifferentiationMuscle SmoothMiddle Agedmusculoskeletal systemmedicine.diseaseSettore MED/40 - Ginecologia E OstetriciaImmunohistochemistrymedicine.anatomical_structureGene Expression RegulationPremenopauseReceptors EstrogenReproductive MedicineReceptors Oxytocinsmooth muscle actinImmunohistochemistryFemaleDesminPeritoneumReceptors ProgesteronebusinessHumanHuman Reproduction
researchProduct

Deletion of myosin VI causes slow retinal optic neuropathy and age-related macular degeneration (AMD)-relevant retinal phenotype

2015

The unconventional myosin VI, a member of the actin-based motor protein family of myosins, is expressed in the retina. Its deletion was previously shown to reduce amplitudes of the a- and b-waves of the electroretinogram. Analyzing wild-type and myosin VI-deficient Snell’s Waltzer mice in more detail, the expression pattern of myosin VI in retinal pigment epithelium, outer limiting membrane, and outer plexiform layer could be linked with differential progressing ocular deficits. These encompassed reduced a-waves and b-waves and disturbed oscillatory potentials in the electroretinogram, photoreceptor cell death, retinal microglia infiltration, and formation of basal laminar deposits. A pheno…

Genotypegenetic structuresOuter retinaTranslocator protein TSPOOuter plexiform layermacromolecular substancesBiologyRetinaPhotoreceptor cellMouse modelStereociliaMacular DegenerationMiceCellular and Molecular Neurosciencechemistry.chemical_compoundOptic Nerve DiseasesMyosinmedicineAnimalsBipolar cellMolecular BiologyPharmacologyRetinaRetinal pigment epitheliumMyosin Heavy ChainsNeurodegenerationInner retinaChoriocapillarisRetinalCell BiologyAnatomyMacular degenerationmedicine.diseaseSynapseeye diseasesCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryMolecular MedicineMicrogliasense organsGene DeletionResearch ArticlePhotoreceptor Cells VertebrateCellular and Molecular Life Sciences
researchProduct

Effect of aging and hypertension on β-myosin heavy chain in heart of spontaneously hypertensive rats

2001

During aging rat myocardium undergoes structural changes characterized by a shift in the synthesis of myosin heavy chain (MHC) from V1 isoform, composed of two alpha-MHC, to V3 isoform, composed of two beta-MHC. In rat, besides ageing, cardiac hypertrophy as adaptive response to a superimposed pressure load (such as hypertension) is characterized by predominance of V3 myosin isoform. The aim of our study was to evaluate the expression of beta-MHC in right (RV) and left (LV) ventricles of spontaneously hypertensive rats (SHRs), a well defined animal model of hypertension, in relation to aging. We used very young (8-week old) and young (15-week old) SHRs and age-matched normotensive Harlan Sp…

MaleGene isoformSenescenceAgingmedicine.medical_specialtyHeart VentriclesBlotting WesternAnimal modelRats Inbred SHRInternal medicineMyosinGeneticsmedicineAnimalsProtein Isoformscardiovascular diseasesMyosin Heavy ChainsOncogenebusiness.industryGeneral MedicineMolecular medicineRatsEndocrinologyApoptosisAgeingHypertensionbusinessInternational Journal of Molecular Medicine
researchProduct

Expression of thyroid hormone receptor isoforms in the hypertrophic heart of spontaneously hypertensive rats

2001

Thyroid hormones (THs) enhance MHC alpha gene- and repress MHC beta gene-transcription in the heart, by interacting with specific nuclear receptors (TRs), that bind to regulatory sequences localized upstream of basal promoter of myosin heavy chain (MHC) genes. The overall effects of THs include an increase in V1- and a decrease in V3-myosin isozyme concentration in the heart. Myosin V1 contains two MHC alpha chains and has a higher ATPase activity than V3 isoform, which contains two beta chains. Previous studies on papillary muscles of spontaneously hypertensive rats (SHRs) showed that heart hypertrophy is accompanied by a shift from alpha to beta MHC accumulation. The present study was aim…

MaleGene isoformmedicine.medical_specialtyHeart VentriclesBlotting WesternAlpha (ethology)CardiomegalyBiologyIsozymeRats Sprague-DawleyRats Inbred SHRInternal medicineMyosinGeneticsmedicineAnimalsProtein IsoformsReceptorReceptors Thyroid HormoneThyroid hormone receptorMyosin Heavy ChainsGeneral MedicineRatsBlotEndocrinologyNuclear receptorHypertensionModels AnimalInternational Journal of Molecular Medicine
researchProduct

Novel slow-skeletal myosin (MYH7) mutation in the original myosin storage myopathy kindred

2006

Abstract Myosin storage myopathy (OMIM 608358), a congenital myopathy characterised by subsarcolemmal, hyaline-like accumulations of myosin in Type I muscle fibres, was first described by Cancilla and Colleagues in 1971 [Neurology 1971;21:579–585] in two siblings as ‘familial myopathy with probable lysis of myofibrils in type I muscle fibres'. Two mutations in the slow skeletal myosin heavy chain gene ( MYH7 ) have recently been associated with the disease in other families. We have identified a novel heterozygous Leu1793Pro mutation in MYH7 in DNA from paraffin sections of one of the original siblings. This historical molecular analysis confirms the original cases had myosin storage myopat…

MaleHeterozygotemacromolecular substancesMyosinsBiologymedicine.disease_causeMuscular DiseasesMyofibrilsMyosinmedicineHumansMyopathyGeneGenetics (clinical)GeneticsMutationMyosin Heavy ChainsMyosin storage myopathyDNAExonsmedicine.diseaseMolecular biologyCongenital myopathyMuscle Fibers Slow-TwitchNeurologyChild PreschoolMutationPediatrics Perinatology and Child HealthFemaleMYH7Neurology (clinical)medicine.symptomMyofibrilCardiac MyosinsNeuromuscular Disorders
researchProduct

Compliance and Pulse Wave Velocity Assessed by MRI Detect Early Aortic Impairment in Young Patients With Mutation of the Smooth Muscle Myosin Heavy C…

2008

Purpose To evaluate aortic elasticity with MRI on young asymptomatic individuals with mutation of the smooth muscle myosin heavy chain in whom aortic enlargement is not present. Materials and Methods Aortic compliance, aortic distensibility, and pulse wave velocity (PWV) were semiautomatically measured from MRI in 8 asymptomatic subjects having a mutation of the MYH11 gene (M+) and 21 nonmutated relatives (M−) of similar age, sex, and blood pressure characteristics. Results Despite a similar aortic diameter in both groups, the aortic compliance and distensibility were significantly lower in M+ subjects compared with M− (0.84 ± 0.33 versus 2.03 ± 0.54 mm2/mmHg, 1.18 ± 0.62 10−3 versus 5.11 ±…

MalePulsatile flow030204 cardiovascular system & hematology030218 nuclear medicine & medical imaging0302 clinical medicinemagnetic resonance imaginggeneticsPulse wave velocityComputingMilieux_MISCELLANEOUSmedicine.diagnostic_test[ INFO.INFO-IM ] Computer Science [cs]/Medical ImagingPrognosisPulsatile FlowAortic valve stenosiscardiovascular systemCardiologyElasticity Imaging TechniquesFemalemedicine.symptomAlgorithmsBlood Flow VelocityAdultmedicine.medical_specialtypulse wave velocityAortic Valve InsufficiencySensitivity and SpecificityAsymptomaticYoung Adult03 medical and health sciencesElastic Modulusmedicine.arteryInternal medicineImage Interpretation Computer-Assistedmedicine[INFO.INFO-IM]Computer Science [cs]/Medical ImagingHumansGenetic Predisposition to DiseaseRadiology Nuclear Medicine and imagingAortaMyosin Heavy ChainsReceiver operating characteristicbusiness.industryReproducibility of ResultsMagnetic resonance imagingAortic Valve StenosisImage Enhancementmedicine.diseaseaortaBlood pressureMutationelasticitybusiness
researchProduct

De-novo Williams–Beuren and inherited Marfan syndromes in a patient with developmental delay and lens dislocation

2017

MaleWilliams Syndrome0301 basic medicinePediatricsmedicine.medical_specialtyGenotypeDevelopmental DisabilitiesFibrillin-1DNA Mutational AnalysisMarfan SyndromePathology and Forensic Medicine03 medical and health sciencesDislocation (syntax)medicineHumansChildAllelesIn Situ Hybridization FluorescenceGenetics (clinical)Myosin Heavy Chainsbusiness.industryFaciesGeneral MedicineLens SubluxationPhenotype030104 developmental biologymedicine.anatomical_structureLens (anatomy)MutationPediatrics Perinatology and Child HealthAnatomybusinessClinical Dysmorphology
researchProduct