Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE25306 | GEO | 2011/02/04

SECONDARY ACCESSION(S): PRJNA134795

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

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

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

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

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

| PRJEB20978 | ENA

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

The effects of muscular dystrophy, exercise and sActRIIB-Fc on molecular signature of skeletal muscle in mice

2014-10-13 | GSE52766 | GEO

The effects of muscular dystrophy, exercise and sActRIIB-Fc on molecular signature of skeletal muscle in mice

Project description:To study the combined effect of myostatin/activin inhibition and exercise on muscle mass and pathophysiology, young mdx mice, a model for Duchenne Muscular Dystrophy, were injected with soluble activin receptor-Fc (sActRIIB-Fc) or placebo (PBS) 1x/week for a 7-week period, in combination with or without voluntary running. C57Bl/10ScSnJ mice injected with PBS acted as wildtype controls. Microarray expression analysis from skeletal muscle was performed using m. gastrocnemies as the sample. We found thatexercise or a combination of exercise and sActRIIB-Fc treatment is more effective in correcting gene expression profiles of dystrophic muscles than the sActRIIB-Fc treatment alone. We also identified several pathways and proteins that were affected by exercise and sActRIIB-Fc together or independently. Total RNA obtained from gastrocnemius muscle of mdx mice divided into four groups: 1) control (injected with PBS, n=5), 2) runners (voluntary wheel running for 7 weeks, injected with PBS, n=5), 3) sActRIIB-Fc -treated (n=5), and 4) runners with sActRIIB-Fc-treatment (n=5). sActRIIB-Fc or PBS was injected intraperitoneally once a week with a 5-mg/kg dose of sActRIIB-Fc. In addition, wildtype mice served as healthy controls (n=4).

2014-10-13 | E-GEOD-52766 | biostudies-arrayexpress

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. Affymetrix Mouse Exon 1.0 ST arrays were hybridized in three biologically independent experiments with RNA from quadriceps muscles of wt, Dysf-/-, F66, F66;Dysf-/- mice, and ACVR2B/Fc-injected wt and Dysf-/- mice at the age of 10 weeks (3 duplicates in 6 different groups, 18 samples).

2015-09-04 | E-GEOD-62945 | biostudies-arrayexpress

Real-Time Quantitative PCR Analyis of Neonatal Rat Whisker Pad Skin-derived Precursors (SKPs)

Project description:Progenitor/stem cell populations of the aorta have been poorly characterized and their self-renewal factors unknown. In this report, we demonstrate that sphere forming progenitor/stem cells, here within termed aortic neurospheres (ANS), can be cultivated from the aorta that are similar to skin-derived precursors (SKPs). Extensive mRNA transcript profiling revealed that ANS abundantly expressed the Inhibin βA transcript, of which the secreted protein dominantly formed the Inhibin βA-βA complex, or Activin A, in the proliferation medium. Co-localization of Activin A, Nestin and Sox2 was observed in the adventitial and peri-adventitial regions of the aorta, indicative of a progenitor/stem cell niche in vivo. Blockade of Activin A signaling, through the neutralization of the Type II Activin receptors ActRIIA and ActRIIB, resulted in the asymmetric differentiation, and epithelial-to-mesenchymal transition of the ANS, respectively. When treated with the latter neutralizing antibody, translocation of the ActRIIB receptor to the nucleus was observed in cells on the periphery of the sphere. Examination of the ActRIIB protein sequence showed the presence of a putative nuclear localization signal of the PY family that was conserved across species. The results from this study demonstrate that Activin A is a self-renewal factor required for maintaining ANS progenitor/stem cell identity and multipotency.

2022-07-05 | GSE207384 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data