Tibialis anterior muscle of myostatin null mice treated with clenbuterol
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE27577 | GEO | 2014/02/03
SECONDARY ACCESSION(S): PRJNA138385
REPOSITORIES: GEO
Similar Datasets
Project description:Transcription profiling of skeletal muscle (tibialis anterior) of 5-week-old male wild type and myostatin null mice given ad libitum access to 20ppm clenbuterol hydrochloride in drinking water or plain tap water for 2 weeks. The objective of the study was to determine overlap in the mechanisms of muscle hypertrophy of the two models. 2x2 factorial arrangement of genotype (wild type and myostatin null) and clenbuterol treatment (control and clenbuterol at 20 ppm) with 4 replicates.
2014-02-03 | E-GEOD-27577 | biostudies-arrayexpress
Project description:Tibialis anterior muscle of myostatin null mice treated with clenbuterol
| PRJNA138385 | ENA
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
Project description:Clenbuterol-HCL can greatly reduce fat deposition and increase skeletal muscle growth at high dosages. In order to advance our understanding of the fundamental molecular mechanisms, Genechips were used to study the differential gene expression profiles of liver tissues among the pigs with/without Clenbuterol-HCL. Differentially expressed genes identified will be the candidates for further investigations on the molecular mechanisms involved in Clenbuterol-HCL of exerting repartition effects on adipose and skeletal muscle tissue.
2010-07-01 | GSE13786 | GEO
Project description:Background: Beta-adrenergic receptor agonists (BA) induce skeletal muscle hypertrophy, yet specific mechanisms that lead to this effect are not well understood. The objective of this research was to identify novel genes and physiological pathways that potentially facilitate BA induced skeletal muscle growth. We chose to evaluate global changes in gene expression by utilizing the Affymetrix platform to identify gene expression changes in mouse skeletal muscle. Changes in gene expression were evaluated 24 h (1D) and 10 days (10D) after administration of the BA clenbuterol. Results: Administration of clenbuterol stimulated anabolic activity, as indicated by decreased blood urea nitrogen (BUN; P < 0.01) and increased body weight gain (P < 0.05) 24 h or 10 d, respectively, after initiation of clenbuterol treatment. A total of 22,787 probesets were evaluated with 113 probesets defined as differentially expressed based on a false discovery rate of 10%. Differential mRNA abundance of four of these genes was validated in an independent experiment by quantitative PCR. Patterns of gene expression change observed from the microarray data suggested more genes are differentially regulated after 24 h than 10 d of BA administration. Functional characterization of differentially expressed genes revealed several categories that participate in biological processes important to skeletal muscle growth, including regulators of transcription and translation, mediators of cell-signaling pathways, and genes involved in polyamine metabolism. Included within these lists were several genes previously associated with myogenic differentiation, along with multiple genes known to promote a general up-regulation of translation. Conclusions: Global evaluation of gene expression after administration of clenbuterol identified changes gene expression and overrepresented functional categories of genes that may regulate BA-induced muscle hypertrophy. Changes in the mRNA abundance of multiple genes associated with myogenic differentiation may indicate an important effect of BA on the proliferation, differentiation, and/or recruitment of satellite cells into muscle fibers to promote muscle hypertrophy. Additionally, increased mRNA abundance of genes involved in the initiation of translation suggests that increased levels of protein synthesis often associated with BA administration may result from a general up-regulation of translational initiators, rather than a sustained up-regulation of gene expression at the transcriptional level. Additionally, numerous other genes and physiological pathways were identified that will be important targets for further investigations of the hypertrophic effect of BA on skeletal muscle. Keywords: Compound administration, time course
2006-03-18 | GSE4490 | GEO
Project description:Clenbuterol-HCL can greatly reduce fat deposition and increase skeletal muscle growth at high dosages. In order to advance our understanding of the fundamental molecular mechanisms, Genechips were used to study the differential gene expression profiles of liver tissues among the pigs with/without Clenbuterol-HCL. Differentially expressed genes identified will be the candidates for further investigations on the molecular mechanisms involved in Clenbuterol-HCL of exerting repartition effects on adipose and skeletal muscle tissue. 4 Chinese mininature pigs were broken into 2 groups with each group having two full sib pigs with the same gender. For the following 8 weeks, test pigs were fed 25 mg/kg clenbuterol twice daily in their diets for 4 weeks and 50 mg/kg clenbuterol for another 4 weeks. The vehicle control pigs were administered in the same manner except that no clenbuterol was added in their diets. The liver expression profiles of 4 pigs were analyzed using Porcine Genome GeneChip. After hybridization, genechips were washed and stained in the Affymetrix Fluidics Station 400 and scanned by using Hewlett-Packard GeneArray Scanner G2500A.
2010-07-30 | E-GEOD-13786 | biostudies-arrayexpress
Project description:Inhibition of myostatin signaling induces strong skeletal muscle growth making it an attractive target to treat muscle wasting and sarcopenia. However, the biological function of myostatin in the heart is barely understood. We demonstrate that conditional inactivation of myostatin in the adult murine heart leads to cardiac hypertrophy, heart failure and increased lethality. To induce cardiomyocyte specific loss of myostatin a conditionally active Mstn^fl/fl allele was generated by insertion of loxP elements upstream and downstream of exons 1 and 2 of the mouse myostatin gene. The selection cassette was removed in vivo by flp-recombination. To inactivate myostatin, mice were mated to alphaMyHC-MCM mice (Sohal, DS, et al. (2001) Circulation Research 89, 20-25). Cre-recombination was achieved by intraperitoneal administration of Tamoxifen (40 mg/kg) for 5 consecutive days. The respective control alphaMyHC-MCM animals were equally treated.
2014-05-16 | E-MEXP-3744 | biostudies-arrayexpress
Project description:Proteomic study of tibialis anterior muscle harvested at 1 day and 7 days post-injection with novel polyurethane nanoparticles compared to water sham and non-injected controls
2021-03-12 | MSV000087040 | MassIVE
Project description:Background: Beta-adrenergic receptor agonists (BA) induce skeletal muscle hypertrophy, yet specific mechanisms that lead to this effect are not well understood. The objective of this research was to identify novel genes and physiological pathways that potentially facilitate BA induced skeletal muscle growth. We chose to evaluate global changes in gene expression by utilizing the Affymetrix platform to identify gene expression changes in mouse skeletal muscle. Changes in gene expression were evaluated 24 h (1D) and 10 days (10D) after administration of the BA clenbuterol. Results: Administration of clenbuterol stimulated anabolic activity, as indicated by decreased blood urea nitrogen (BUN; P < 0.01) and increased body weight gain (P < 0.05) 24 h or 10 d, respectively, after initiation of clenbuterol treatment. A total of 22,787 probesets were evaluated with 113 probesets defined as differentially expressed based on a false discovery rate of 10%. Differential mRNA abundance of four of these genes was validated in an independent experiment by quantitative PCR. Patterns of gene expression change observed from the microarray data suggested more genes are differentially regulated after 24 h than 10 d of BA administration. Functional characterization of differentially expressed genes revealed several categories that participate in biological processes important to skeletal muscle growth, including regulators of transcription and translation, mediators of cell-signaling pathways, and genes involved in polyamine metabolism. Included within these lists were several genes previously associated with myogenic differentiation, along with multiple genes known to promote a general up-regulation of translation. Conclusions: Global evaluation of gene expression after administration of clenbuterol identified changes gene expression and overrepresented functional categories of genes that may regulate BA-induced muscle hypertrophy. Changes in the mRNA abundance of multiple genes associated with myogenic differentiation may indicate an important effect of BA on the proliferation, differentiation, and/or recruitment of satellite cells into muscle fibers to promote muscle hypertrophy. Additionally, increased mRNA abundance of genes involved in the initiation of translation suggests that increased levels of protein synthesis often associated with BA administration may result from a general up-regulation of translational initiators, rather than a sustained up-regulation of gene expression at the transcriptional level. Additionally, numerous other genes and physiological pathways were identified that will be important targets for further investigations of the hypertrophic effect of BA on skeletal muscle. Experiment Overall Design: A total of 27 mice were used to represent three treatments. Hybridizations were done using RNA pools from 3 mice, with 3 pools (replicates) per treatment. Treatments included control, 1 day of clenbuterol administration, and 10 days of clenbuterol administration. Data represent skeletal muscle gene expression.
2008-06-13 | E-GEOD-4490 | biostudies-arrayexpress
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