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Comparing effects of inhibition of activin receptor type IIB (ActRIIB), myostatin (GDF8) and/or activinA in mouse muscle

ABSTRACT: Comparing effects of inhibition of activin receptor type IIB (ActRIIB), myostatin (GDF8) and/or activinA in mouse muscle

PROVIDER: PRJEB20978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1989950.fastq.gz	Fastqsanger.gz
	ERR1989960.fastq.gz	Fastqsanger.gz
	ERR1989970.fastq.gz	Fastqsanger.gz
	ERR1989980.fastq.gz	Fastqsanger.gz
	ERR1989951.fastq.gz	Fastqsanger.gz

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Comparing effects of inhibition of activin receptor type IIB (ActRIIB), myostatin (GDF8) and/or activinA in mouse muscle

Project description:This study was to compare the gene expression of our anti-GDF8 (i.e. anti-myostatin) and anti-activin A antibody combination to that of the activin receptor type IIB (ActRIIB.hFc) trap in SCID mice. The study was conducted in tibialis anterior muscle that is a common muscle type for the hypertrophy study. The combination treatment produces very similar muscle growth in tibialis muscle as the ActRIIB.hFc trap, however our combination blocks two specific ligands compared to the many ligands the receptor trap will inhibit. The difference in gene expression between these groups demonstrates that despite producing similar muscle growth, the trap affecting more genes in muscle without producing additional muscle hypertrophy.

2017-06-01 | E-MTAB-4943 | biostudies-arrayexpress

Gene expression profiling of skeletal muscles treated with a soluble activin type IIB receptor

2011-02-04 | GSE25306 | GEO

Gene expression profiling of skeletal muscles treated with a soluble activin type IIB receptor

Project description:Inhibition of the myostatin signaling pathway is emerging as a promising therapeutic means to treat muscle wasting disorders. Activin type IIB receptor is the putative myostatin receptor, and a soluble activin receptor (ActRIIB-Fc) has been demonstrated to potently inhibit a subset of TGF-β family members including myostatin. In order to determine reliable and valid biomarkers for myostatin pathway inhibition, we assessed gene expression profiles for quadriceps muscles from mice treated with ActRIIB-Fc compared to mice genetically lacking myostatin and control mice. RNA extracted from quadriceps muscles of four classes of two-month-old female mice were analyzed with Affymetrix microarrays: control mice, myostatin-null mice, mice treated with one dose of ActRIIB-Fc and mice treated with four doses of ActRIIB-Fc. An initial study used 3 mice from each class, and an independent follow-up study used 8 myostatin-null mice and 5 mice from each of the other 3 classes.

2011-02-04 | E-GEOD-25306 | biostudies-arrayexpress

Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight

Project description:Among the physiological consequences of extended space flight are loss of skeletal muscle and bone mass. One signaling pathway that plays an important role in maintaining muscle and bone homeostasis is that regulated by the secreted signaling proteins, myostatin and activin A. Here, we used both pharmacological and genetic approaches to investigate the effect of targeting myostatin/activin A signaling in mice that were sent to the International Space Station. We show that inhibition of myostatin/activin A signaling has a significant protective effect against microgravity-induced muscle and bone loss. These findings have implications for therapeutic strategies to combat the concomitant muscle and bone loss occurring in people afflicted with disuse atrophy on Earth as well as in astronauts in space, especially during prolonged missions.

2020-09-16 | GSE156321 | GEO

The effects of doxorubicin and blocking activin receptor 2B ligands in mice [muscle]

Project description:Doxorubicin is a widely used and effective anthracycline chemotherapy drug. However, it causes cardiotoxicity and also a few negative effects on skeletal muscle as well. As a result, cancer treatment might actually worsen cancer-induced cachexia and consequently the prognosis of the disease. Inhibiting myostatin/activin signaling is known to increase muscle size. This pathway blockade by soluble activin receptor IIB (sAcvR2B-Fc) has also prolonged survival in cancer, even of animals in which tumor growth is not inhibited. It is not known, however, whether blocking this pathway affects chemotherapy-induced muscle wasting. We found that doxorubicin induces muscle atrophy which is prevented by a blocker for activin receptor 2B ligands (sAcvR2B-Fc).

2016-09-25 | GSE77745 | GEO

The effects of doxorubicin and blocking activin receptor 2B ligands in mice [heart]

2017-12-04 | GSE97642 | GEO

Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington’s disease mice.

Project description:Huntington’s disease (HD) is an inherited neurodegenerative disorder of which skeletal muscle atrophy is a common feature, and multiple lines of evidence support a muscle-based pathophysiology in HD mouse models. Inhibition of myostatin signaling increases muscle mass, and therapeutic approaches based on this are in clinical development. We have used a soluble ActRIIB decoy receptor (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model of HD. Transcriptional profiling of muscle in treated and untreated wild-type and R6/2 mice was performed to analyze the effect of the ActRIIB decoy on genes and pathways involved in maintaining normal muscle physiology as well as those dysregulated due to the mutant HTT gene mutation.

2017-10-29 | GSE81367 | GEO

Skeletal muscle gene expression after myostatin knockout in mature mice

Project description:RNA from 5 mice with postdevelopmental knockout of myostatin and 5 mice with normal myostatin expression was analyzed with comprehensive oligonucleotide microarrays. Myostatin depletion affected the expression of several hundred genes at nominal P < 0.01, but fewer than a hundred effects were statistically significant according to a more stringent criterion (false discovery rate < 5%). Most of the effects were less than 1.5-fold in magnitude. In contrast to previously-reported effects of constitutive myostatin knockout, postdevelopmental knockout did not downregulate expression of genes encoding slow isoforms of contractile proteins or genes encoding proteins involved in energy metabolism. Several collagen genes were expressed at lower levels in the myostatin-deficient muscles, and this led to reduced tissue collagen levels as reflected by hydroxyproline content. Myostatin knockout tended to down-regulate the expression of sets of genes with promoter motifs for Smad3, Smad4, myogenin, NF-κB, serum response factor, and numerous other transcription factors. Main conclusions: in mature muscle, myostatin is a key transcriptional regulator of collagen genes, but not genes encoding contractile proteins or genes encoding proteins involved in energy metabolism.

2009-03-24 | GSE15349 | GEO

Muscle Hypertrophy Induced by Myostatin Inhibition Accelerates Degeneration in Dysferlinopathy

Project description:Because myostatin normally limits skeletal muscle growth, there is an extensive effort to develop myostatin inhibitors for clinical use. One potential concern is that in patients with muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic fibers. Here, we show that blocking the myostatin pathway in dysferlin mutant mice results in early improvement in histopathology but ultimately accelerates muscle degeneration. Hence, benefits of this approach should be weighed against these potential detrimental effects.

2015-09-04 | GSE62945 | GEO

Soluble activin receptor type IIB decoy receptor differentially impacts murine osteogenesis imperfecta muscle function.

Project description:INTRODUCTION:Osteogenesis imperfecta (OI) is characterized by skeletal fragility and muscle weakness. In this study we investigated the effects of soluble activin type IIB receptor (sActRIIB-mFc) on muscle mass and function in 2 distinct mouse models of OI: osteogenesis imperfecta murine (oim) and +/G610C. METHODS:Wild-type (WT), +/G610C, and oim/oim mice were treated from 2 to 4 months of age with Tris-buffered saline (vehicle) or sActRIIB-mFc and their hindlimb muscles evaluated for mass, morphology, and contractile function. RESULTS:sActRIIB-mFc-treated WT, +/G610C, and oim/oim mice had increased hindlimb muscle weights and myofiber cross-sectional area compared with vehicle-treated counterparts. sActRIIB-mFc-treated oim/oim mice also exhibited increased contractile function relative to vehicle-treated counterparts. DISCUSSION:Blocking endogenous ActRIIB was effective at increasing muscle size in mouse models of OI, and increasing contractile function in oim/oim mice. ActRIIB inhibitors may provide a potential mutation-specific therapeutic option for compromised muscle function in OI. Muscle Nerve 57: 294-304, 2018.

| S-EPMC5702601 | biostudies-literature

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