Search results for "Activin Receptors"

showing 10 items of 15 documents

Muscle and serum metabolomes are dysregulated in colon-26 tumor-bearing mice despite amelioration of cachexia with activin receptor type 2B ligand bl…

2019

Cancer-associated cachexia reduces survival, which has been attenuated by blocking the activin receptor type 2B (ACVR2B) ligands in mice. The purpose of this study was to unravel the underlying physiology and novel cachexia biomarkers by use of the colon-26 (C26) carcinoma model of cancer cachexia. Male BALB/c mice were subcutaneously inoculated with C26 cancer cells or vehicle control. Tumor-bearing mice were treated with vehicle (C26+PBS) or soluble ACVR2B either before (C26+sACVR/b) or before and after (C26+sACVR/c) tumor formation. Skeletal muscle and serum metabolomics analysis was conducted by gas chromatography-mass spectrometry. Cancer altered various biologically functional groups …

0301 basic medicineMaleCachexiaPhysiologyEndocrinology Diabetes and MetabolismActivin Receptors Type IIlihaksetMyostatinMice0302 clinical medicineAmino Acidsta315Activin Receptor Type-2BbiologyOrganophosphatesRecombinant Proteins3. Good healthmedicine.anatomical_structureribosome030220 oncology & carcinogenesismyostatinColonic NeoplasmsMetabolomesyöpätauditC26Metabolic Networks and Pathwaysmedicine.medical_specialtyPhenylalanineCachexia03 medical and health sciencesribosomitPhysiology (medical)Internal medicineCell Line TumormedicineAnimalsskeletal muscleMuscle SkeletalPI3K/AKT/mTOR pathwaybusiness.industrySkeletal muscleCancermedicine.diseaseta3122BlockadeImmunoglobulin Fc Fragments030104 developmental biologyEndocrinologyProtein Biosynthesisbiology.proteinaineenvaihduntatuotteetPyrimidine NucleotidesproteiinitbusinesslihassurkastumasairaudetACVR2BAmerican journal of physiology. Endocrinology and metabolism
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Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

2016

Protein homeostasis in cells, proteostasis, is maintained through several integrated processes and pathways and its dysregulation may mediate pathology in many diseases including Duchenne muscular dystrophy (DMD). Oxidative stress, heat shock proteins, endoplasmic reticulum (ER) stress and its response, i.e. unfolded protein response (UPR), play key roles in proteostasis but their involvement in the pathology of DMD are largely unknown. Moreover, exercise and activin receptor IIB blocking are two strategies that may be beneficial to DMD muscle, but studies to examine their effects on these proteostasis pathways are lacking. Therefore, these pathways were examined in the muscle of mdx mice, …

0301 basic medicineX-Box Binding Protein 1Activin Receptors Type IIEukaryotic Initiation Factor-2MyostatinUPRBiochemistryMiceeIF-2 KinaseThioredoxinsSirtuin 1ENDOPLASMIC-RETICULUM STRESSDISULFIDE-ISOMERASEPhosphorylationta315Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsIN-VIVOta3141Activin receptorMOUSE MODELER STRESSEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structuremyostatinPRESERVES MUSCLE FUNCTIONER-stressSKELETAL-MUSCLEmdxSignal TransductionEXPRESSIONmedicine.medical_specialtyXBP1MDX MICEBiologyProtein Serine-Threonine Kinases03 medical and health sciencesPhysiology (medical)Internal medicineHeat shock proteinPhysical Conditioning AnimalEndoribonucleasesmedicineAnimalsHumansRNA MessengerMuscle SkeletalSkeletal muscleMyostatinGENEActivating Transcription Factor 6Immunoglobulin Fc FragmentsMuscular Dystrophy DuchenneDisease Models Animal030104 developmental biologyProteostasisEndocrinologyGene Expression RegulationUnfolded protein responsebiology.proteinMice Inbred mdxProteostasisUnfolded Protein Response3111 BiomedicineCarrier ProteinsACVR2B
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Luspatercept for the treatment of anaemia in patients with lower-risk myelodysplastic syndromes (PACE-MDS): a multicentre, open-label phase 2 dose-fi…

2017

Myelodysplastic syndromes are characterised by ineffective erythropoiesis. Luspatercept (ACE-536) is a novel fusion protein that blocks transforming growth factor beta (TGF β) superfamily inhibitors of erythropoiesis, giving rise to a promising new investigative therapy. We aimed to assess the safety and efficacy of luspatercept in patients with anaemia due to lower-risk myelodysplastic syndromes.In this phase 2, multicentre, open-label, dose-finding study (PACE-MDS), with long-term extension, eligible patients were aged 18 years or older, had International Prognostic Scoring System-defined low or intermediate 1 risk myelodysplastic syndromes or non-proliferative chronic myelomonocytic leuk…

AdultMaleIneffective erythropoiesismyalgiamedicine.medical_specialtyPediatricsTime FactorsMaximum Tolerated DoseAnemiaActivin Receptors Type IIRecombinant Fusion ProteinsKaplan-Meier EstimateLower riskmedicine.disease_causeRisk AssessmentSeverity of Illness IndexDisease-Free SurvivalDrug Administration Schedule03 medical and health sciences0302 clinical medicineGermanyInternal medicineSeverity of illnessmedicineHumansProspective StudiesProspective cohort studyAdverse effectAgedProportional Hazards ModelsDose-Response Relationship Drugbusiness.industryMyelodysplastic syndromesAnemiaMiddle AgedPrognosismedicine.diseaseSurvival AnalysisActivinsImmunoglobulin Fc FragmentsTreatment OutcomeOncologyMyelodysplastic Syndromes030220 oncology & carcinogenesisFemalemedicine.symptombusiness030215 immunologyThe Lancet Oncology
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Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyActivin Receptors Type IIMyocardial IschemiaMyostatinBiochemistryMuscle hypertrophyMice03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineAnimalsMyocyteMyocardial infarctionMolecular BiologyVentricular Remodelingbiologybusiness.industrySkeletal muscleHeartmedicine.disease3. Good healthBlockadeMice Inbred C57BLDisease Models AnimalMuscular Atrophy030104 developmental biologymedicine.anatomical_structureCardiologybiology.proteinbusiness030217 neurology & neurosurgeryACVR2BSignal TransductionTranscription FactorsBiotechnologyThe FASEB Journal
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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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Muscle NAD+ depletion and Serpina3n as molecular determinants of murine cancer cachexia—the effects of blocking myostatin and activins

2020

Objective Cancer cachexia and muscle loss are associated with increased morbidity and mortality. In preclinical animal models, blocking activin receptor (ACVR) ligands has improved survival and prevented muscle wasting in cancer cachexia without an effect on tumour growth. However, the underlying mechanisms are poorly understood. This study aimed to identify cancer cachexia and soluble ACVR (sACVR) administration-evoked changes in muscle proteome. Methods Healthy and C26 tumour-bearing (TB) mice were treated with recombinant sACVR. The sACVR or PBS control were administered either prior to the tumour formation or by continued administration before and after tumour formation. Muscles were an…

MaleEXPRESSIONActivin receptor; APR; C26; Cancer cachexia; Nrk2; OXPHOSlcsh:Internal medicineCachexiaREVERSALActivin ReceptorsMETABOLISMactivin receptorOxidative PhosphorylationCell Line TumorAnimalsMuscle Skeletallcsh:RC31-1245aineenvaihduntaSerpinslihassolut318 Medical biotechnologyNrk2Cancer cachexiaMyostatinNADOXPHOSMUSCULAR-DYSTROPHYActivinsMitochondriaActivin receptorDisease Models AnimalMuscular AtrophyMICESIRTUINSOriginal ArticlesyöpätauditproteiinitC26lihassurkastumasairaudetAPRAcute-Phase Proteinscancer cachexia
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Treating cachexia using soluble ACVR2B improves survival, alters mTOR localization, and attenuates liver and spleen responses.

2018

Background Cancer cachexia increases morbidity and mortality, and blocking of activin receptor ligands has improved survival in experimental cancer. However, the underlying mechanisms have not yet been fully uncovered. Methods The effects of blocking activin receptor type 2 (ACVR2) ligands on both muscle and non‐muscle tissues were investigated in a preclinical model of cancer cachexia using a recombinant soluble ACVR2B (sACVR2B‐Fc). Treatment with sACVR2B‐Fc was applied either only before the tumour formation or with continued treatment both before and after tumour formation. The potential roles of muscle and non‐muscle tissues in cancer cachexia were investigated in order to understand th…

MaleTUMOR-BEARING MICElcsh:Diseases of the musculoskeletal systemCachexiaprotein synthesisActivin Receptors Type IIMDSCphysical activityAcute phase responseKaplan-Meier EstimateACTIVATIONActivinMiceNeoplasmsOrthopedics and Sports MedicineTOR Serine-Threonine Kinasesactivinlcsh:Human anatomyII RECEPTORSRecombinant ProteinsProtein TransportLivermyostatinPROTEIN-SYNTHESISSKELETAL-MUSCLECytokinessyöpätauditInflammation MediatorsACUTE-PHASE RESPONSE3122 CancersINHIBITIONlcsh:QM1-695acute phase responsePhysiology (medical)Cell Line TumorAnimalsHumansMuscle SkeletalActivin; Acute phase response; MDSC; Myostatin; Physical activity; Protein synthesis; Orthopedics and Sports Medicine; Physiology (medical)Physical activityMyeloid-Derived Suppressor CellsMyostatinXenograft Model Antitumor AssaysDisease Models AnimalACTIVIN-APHYSICAL-ACTIVITY3121 General medicine internal medicine and other clinical medicineproteiinitEXPERIMENTAL CANCER CACHEXIAlcsh:RC925-935Protein synthesislihassurkastumasairaudetBiomarkersSpleenJournal of cachexia, sarcopenia and muscle
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Prevention of chemotherapy‐induced cachexia by ACVR2B ligand blocking has different effects on heart and skeletal muscle

2017

Background Toxicity of chemotherapy on skeletal muscles and the heart may significantly contribute to cancer cachexia, mortality, and decreased quality of life. Doxorubicin (DOX) is an effective cytostatic agent, which unfortunately has toxic effects on many healthy tissues. Blocking of activin receptor type IIB (ACVR2B) ligands is an often used strategy to prevent skeletal muscle loss, but its effects on the heart are relatively unknown. Methods The effects of DOX treatment with or without pre-treatment with soluble ACVR2B-Fc (sACVR2B-Fc) were investigated. The mice were randomly assigned into one of the three groups: (1) vehicle (PBS)-treated controls, (2) DOX-treated mice (DOX), and (3) …

Malep53Cachexialcsh:Diseases of the musculoskeletal systemActivin Receptors Type IILigandsdoxorubicinCcl21lcsh:QM1-695MiceAnimalsHumanssytostaattihoitoMuscle SkeletalAntibiotics AntineoplasticactivinsHeartOriginal Articleslcsh:Human anatomyMyostatinActivinsDoxorubicinmyostatinQuality of LifeOriginal Articleproteiinittranskriptomilcsh:RC925-935TranscriptomelihassurkastumasairaudetJournal of Cachexia, Sarcopenia and Muscle
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Developmental and tumoral vascularization is regulated by G protein-coupled receptor kinase 2

2012

Tumor vessel dysfunction is a pivotal event in cancer progression. Using an in vivo neovascularization model, we identified G protein–coupled receptor kinase 2 (GRK2) as a key angiogenesis regulator. An impaired angiogenic response involving immature vessels was observed in mice hemizygous for Grk2 or in animals with endothelium-specific Grk2 silencing. ECs isolated from these animals displayed intrinsic alterations in migration, TGF-β signaling, and formation of tubular networks. Remarkably, an altered pattern of vessel growth and maturation was detected in postnatal retinas from endothelium-specific Grk2 knockout animals. Mouse embryos with systemic or endothelium-selective Grk2 ablation …

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Angiogenic SwitchAngiogenesisMedicinaActivin Receptors Type IIMelanoma ExperimentalReceptor Transforming Growth Factor-beta Type INeovascularization PhysiologicProtein Serine-Threonine KinasesBiologyMural cellGrk2Transforming Growth Factor beta1NeovascularizationMiceDownregulation and upregulationCell MovementPregnancyInternal medicinemedicineAnimalsHumansCell ProliferationHemizygoteMice KnockoutG protein-coupled receptor kinaseTumorNeovascularization PathologicEndothelial CellsRetinal VesselsG proteinGeneral MedicineCell biologyEndocrinologymedicine.anatomical_structurecardiovascular systemFemalePericyteSignal transductionmedicine.symptomActivin Receptors Type IReceptors Transforming Growth Factor betaSignal TransductionResearch Article
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