Tibialis anterior muscle of myostatin null mice treated with clenbuterol
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Anna Dilger
PROVIDER: E-GEOD-27577 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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: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.
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2010-09-13 | E-GEOD-20704 | biostudies-arrayexpress
Project description:Glaucoma is not only the second leading cause of blindness worldwide, but patient numbers will also increase significantly in the coming years due to aging societies. Glaucoma is a progressive optic neuropathy with changes at the optic nerve head, gradual retinal ganglion cell (RGC) death, and visual field loss [1]. Unfortunately, glaucoma can remain asymptomatic until it is rather far progressed, hence about 10-50 % of patients are unaware they suffer from this disease. High intraocular pressure (IOP) is the main risk factor; however, normal-tension glaucoma (NTG) occurs in patients with physiological IOP [2]. This form account for about 30 % of glaucoma patients [3]. Furthermore, sustained IOP lowering can slow down, but does not completely stop disease progression in patients. [4, 5]. Additionally, the administration of topical glaucoma medications can lead to side effects, such as ocular irritation, decreasing the compliance of patients. These facts emphasize the importance of discovering new treatment strategies. The exact pathogenesis for glaucoma is still unknown, but several factors are considered to be involved (fig.1). The most prominent factor is an elevated IOP, which can cause blockade of axonal protein transport at the lamina cribrosa, causing an initial axonal damage and RGC death by trophic insufficiency. In addition, ischemic/hypoxic damage [6], astrocyte and glia cell alterations, and excessive stimulation of the glutamatergic system [7] are discussed as possible pathomechanisms. Moreover, an involvement of the immune system is considered [8-10]. In glaucoma patients, up- and downregulations in the systemic and ocular antibody profile were detected [11-13]. Also, antibody deposits were observed in glaucomatous retinae [14]. It is likely that a combination of several pathogenic factors/mechanisms increases the possibility of developing glaucoma. For the investigation of pathomechanisms and novel therapies, it is necessary to have suitable models that allow such screening. To investigate whether antibodies detected in glaucoma patients are part of glaucoma pathogenesis or a result of disease progression, the experimental autoimmune glaucoma (EAG) animal model was established. This animal model is based on the fact that autoantibodies against S100B, a small calcium binding protein expressed in glia cells, were found to be increased in glaucoma patients [15]. In this model, an immunization with S100B led to a significant loss of RGCs after 28 days and a fast degeneration of optic nerves [20]. The IOP in this model was not altered. Therefore, we were able to mimic the effects seen in NTG patients, an IOP-independent glaucomatous degeneration, by immunizing rats with S100B. S100B is a calcium-binding protein. In the central nervous system (CNS), it is mainly expressed by glial cells such as oligodendrocytes, Schwann cells, ependymal cells, retinal Müller cells and astrocytes [16]. S100B regulates and maintains the homeostasis of the important second messenger calcium and is therefore involved in many cell activities, such as signal transduction, cell differentiation, regulation of cell motility, transcription and cell cycle processes [17, 18]. Extracellularly, S100B can act as a signal molecule and bind receptors such as the receptor for advanced glycation end products (RAGE). In high concentrations, S100B can have negative effects and lead to cell death. For example, the binding of RAGE can induce the activation of microglia cells leading to a release of proinflammatory cytokines to an excessive extent [19]. Furthermore, there seems to be a link between S100B and neuronal diseases. In glaucoma patients, high antibody titers against S100B were found [20]. To investigate the effect of S100B in glaucoma more precisely, the immunization with S100B leads to a loss of retinal ganglion cells (RGCs) without an elevation of the IOP after 28 days in the EAG model [21, 22]. The goal of the present study was to detect the retinal biomarkers in EAG animals 7 and 14 days after immunization with S100B. To detect these new markers in disease development, a label free quantitative mass spectrometry-based approach will be used.
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2010-09-14 | E-GEOD-20703 | biostudies-arrayexpress
Project description:The purpose of this study was to determine whether postdevelopmental myostatin depletion influenced the changes in skeletal muscle gene expression profiles induced by a long-term increase in physical activity. Myostatin levels in muscles of adult male mice with floxed myostatin genes were reduced ~85% by activating Cre recombinase. Control mice with normal myostatin genes had the same Cre-activating treatment. Some of the mice were housed in ordinary cages throughout the study, limiting their physical activity. Other mice were given free access to running wheels for the final 12 weeks of the study. At the end of the study, comprehensive gene expression profiles of triceps brachii muscles were determined by RNA sequencing (RNA-Seq), with muscles from mice selected for similarity of running behavior throughout the period of wheel access. Wheel running increased expression of hundreds of mRNAs encoding proteins involved in oxidative energy metabolism, and this response was not affected by myostatin deficiency. The running-induced increase in the ratio of Myh1 mRNA (which encodes myosin heavy chain type 2x) to Myh4 mRNA (which encodes myosin heavy chain type 2b) also was not affected by myostatin depletion. At every threshold of P (computed by analysis of variance), the number of transcripts with interactions between activity level and myostatin level was fewer than the number expected by chance. These data suggest that myostatin is not required for transcriptional adaptations to moderate-intensity exercise. 12 samples, 6 from sedentary mice and 6 from active (wheel running) mice. 3 control and 3 myostatin-deficient mice within each activity level.
2011-09-02 | E-GEOD-31839 | biostudies-arrayexpress