Search results for "Activin receptor"

showing 5 items of 25 documents

Exercise restores decreased physical activity levels and increases markers of autophagy and oxidative capacity in myostatin/activin blocked mdx mice

2013

The importance of adequate levels of muscle size and function and physical activity is widely recognized. Myostatin/activin blocking increases skeletal muscle mass but may decrease muscle oxidative capacity and can thus be hypothesized to affect voluntary physical activity. Soluble activin receptor IIB (sActRIIB-Fc) was produced to block myostatin/activins. Modestly dystrophic mdx mice were injected with sActRIIB-Fc or PBS with or without voluntary wheel running exercise for 7 wk. Healthy mice served as controls. Running for 7 wk attenuated the sActRIIB-Fc-induced increase in body mass by decreasing fat mass. Running also enhanced/restored the markers of muscle oxidative capacity and autoph…

medicine.medical_specialtyPhysiologyActivin Receptors Type IIEndocrinology Diabetes and MetabolismBlotting WesternCitrate (si)-SynthaseMyostatinMotor ActivityHematocritMuscle hypertrophyEatingHemoglobinsMice03 medical and health sciences0302 clinical medicinePhysical Conditioning AnimalPhysiology (medical)Internal medicineAutophagymedicineAnimalsMuscle Skeletalta315Creatine KinaseAdiposity030304 developmental biology0303 health sciencesbiologymedicine.diagnostic_testTumor Necrosis Factor-alphaBody WeightAutophagySkeletal muscleDNAActivin receptorMyostatinActivinsMice Inbred C57BLmedicine.anatomical_structureEndocrinologyHematocritMice Inbred mdxbiology.proteinCreatine kinaseTumor necrosis factor alphaOxidation-Reduction030217 neurology & neurosurgeryAmerican Journal of Physiology-Endocrinology and Metabolism
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Growth and differentiation factor 11 (GDF11): Functions in the regulation of erythropoiesis and cardiac regeneration

2015

International audience; Members of the TGF-β superfamily transduce their signals through type I and II receptor serine/threonine kinases. The binding of activins to activin type IIA (ActRIIA) or type IIB (ActRIIB) receptors induces the recruitment and phosphorylation of an activin type I receptor (ALK4 and/or ALK7), which then phosphorylates the Smad2 and Smad3 intracellular signaling proteins. The regulation of members of the TGF-β family is known to be complex, because many proteins able to bind the ligands and inhibit their activities have been identified. Growth and differentiation factor 11 (Gdf11) belongs to the TGF-β family. GDF11, like other members of the TGF-β superfamily, is prod…

medicine.medical_specialtySmad2 ProteinProtein Serine-Threonine Kinases030204 cardiovascular system & hematologyBiology03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineTGF beta signaling pathway[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansRegeneration[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPharmacology (medical)PhosphorylationCCL11Activin type 2 receptors030304 developmental biologyPharmacology0303 health sciencesR-SMADcardiac regenerationGrowth differentiation factorHeartActivins[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemCell biologyBMPR2Growth Differentiation FactorsEndocrinologyBone Morphogenetic ProteinsGDF11Smad2 ProteinSignal transductionActivin Receptors Type IerythropoiesisACVR2BSignal TransductionPharmacology & Therapeutics
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Myostatin/activin blocking combined with exercise reconditions skeletal muscle expression profile of mdx mice

2015

Duchenne Muscular Dystrophy is characterized by muscle wasting and decreased aerobic metabolism. Exercise and blocking of myostatin/activin signaling may independently or combined counteract muscle wasting and dystrophies. The effects of myostatin/activin blocking using soluble activin receptor-Fc (sActRIIB-Fc) administration and wheel running were tested alone or in combination for seven weeks in dystrophic mdx mice. Expression microarray analysis revealed decreased aerobic metabolism in the gastrocnemius muscle of mdx mice compared to healthy mice. This was not due to reduced home-cage physical activity, and was further downregulated upon sActRIIB-Fc treatment in enlarged muscles. However…

muscular dystrophymedicine.medical_specialtyDuchenne muscular dystrophyActivin Receptors Type IIRecombinant Fusion Proteinsphysical activityMyostatinBiologyta3111BiochemistryMuscle hypertrophy03 medical and health sciencesGastrocnemius muscleMice0302 clinical medicineEndocrinologyoxidative metabolismInternal medicinePhysical Conditioning AnimalGene expressionmedicineSTAT5 Transcription FactorAnimalsmuscle hypertrophyMuscular dystrophyPhosphorylationta315Muscle SkeletalMolecular BiologyWasting030304 developmental biologyInhibin-beta Subunits0303 health sciencesPhysical activitySkeletal muscleMyostatinmusculoskeletal systemmedicine.diseaseMuscular dystrophymRNA profilingEndocrinologymedicine.anatomical_structurebiology.proteinMice Inbred mdxOxidative metabolismMuscle hypertrophymedicine.symptom030217 neurology & neurosurgery
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Combined effect of AAV-U7-induced dystrophin exon skipping and soluble activin Type IIB receptor in mdx mice.

2012

Adeno-associated virus (AAV)-U7-mediated skipping of dystrophin-exon-23 restores dystrophin expression and muscle function in the mdx mouse model of Duchenne muscular dystrophy. Soluble activin receptor IIB (sActRIIB-Fc) inhibits signaling of myostatin and homologous molecules and increases muscle mass and function of wild-type and mdx mice. We hypothesized that combined treatment with AAV-U7 and sActRIIB-Fc may synergistically improve mdx muscle function. Bioactivity of sActRIIB-Fc on skeletal muscle was first demonstrated in wild-type mice. In mdx mice we show that AAV-U7-mediated dystrophin restoration improved specific muscle force and resistance to eccentric contractions when applied a…

musculoskeletal diseasesmdx mousemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesDuchenne muscular dystrophyActivin Receptors Type IIGenetic VectorsMyostatinBiologyDystrophin03 medical and health sciencesMice0302 clinical medicineInternal medicineGeneticsmedicineMyocyteAnimalsMuscular dystrophyMuscle SkeletalMolecular Biology030304 developmental biology0303 health sciencesBody WeightSkeletal muscleExonsGenetic TherapyDependovirusMuscular Dystrophy Animalmedicine.diseasemusculoskeletal system3. Good healthMice Inbred C57BLEndocrinologymedicine.anatomical_structureImmunologybiology.proteinMice Inbred mdxMolecular MedicineITGA7Dystrophin030217 neurology & neurosurgeryMuscle ContractionHuman gene therapy
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Targeting the Activin Receptor Signaling to Counteract the Multi-Systemic Complications of Cancer and Its Treatments

2021

Muscle wasting, i.e., cachexia, frequently occurs in cancer and associates with poor prognosis and increased morbidity and mortality. Anticancer treatments have also been shown to contribute to sustainment or exacerbation of cachexia, thus affecting quality of life and overall survival in cancer patients. Pre-clinical studies have shown that blocking activin receptor type 2 (ACVR2) or its ligands and their downstream signaling can preserve muscle mass in rodents bearing experimental cancers, as well as in chemotherapy-treated animals. In tumor-bearing mice, the prevention of skeletal and respiratory muscle wasting was also associated with improved survival. However, the definitive proof tha…

tumorCachexiaActivin ReceptorsActivin Receptors Type IIMyostatinReviewchemotherapymulti-organType IIsurvivalCachexiaNeoplasmsmedicineRespiratory muscleHumansActivins; Cancer cachexia; Chemotherapy; Mortality; Multi-organ; Muscle wasting; Myostatin; Survival; Tumor; Activin Receptors Type II; Cachexia; Humans; Neoplasms; Signal Transduction; Survival Analysislcsh:QH301-705.5Wastingsoluviestintäbiologysyöpähoidotbusiness.industryactivinsCancerSkeletal musclemuscle wastingGeneral MedicineActivin receptormedicine.diseaseSurvival AnalysismortalityBlockademedicine.anatomical_structurelcsh:Biology (General)myostatinCancer researchbiology.proteinproteiinitmedicine.symptombusinesshenkiinjääminenlihassurkastumasairaudetSignal Transductioncancer cachexia
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