Role of the Cytoskeleton in muscle transcriptional response to altered use
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE41363 | GEO | 2012/10/06
SECONDARY ACCESSION(S): PRJNA176690
REPOSITORIES: GEO
Similar Datasets
Project description:Desmin is a cytoskeletal protein in muscle involved in integrating cellular space and transmitting forces. In this study we sought to determine the combinatory effects of desmin deletion, aging and eccentric exercise on skeletal muscle at the transcriptional level across many pathways of muscle physiology. RNA was isolated from the TA muscle of mice of two genotypes (wildtype (WT) and desmin knockout (KO)) and two ages (7-9 weeks (Adult) and 12-14 months (Aged)). TA muscles were subjected to a bout of 50 eccentric contractions 12 hours prior to RNA isolation. Numbers per group are as follows: WT_Adult (5), WT_Aged (5), KO_Adult (5), KO_Aged (4).
2012-10-06 | E-GEOD-41363 | biostudies-arrayexpress
Project description:Desmin is a cytoskeletal protein in muscle involved in integrating cellular space and transmitting forces. In this study we sought to determine the effects of desmin deletion on skeletal muscle at the transcriptional level across many pathways of muscle physiology.
2012-07-11 | GSE34388 | GEO
Project description:Desmin is a cytoskeletal protein in muscle involved in integrating cellular space and transmitting forces. In this study we sought to determine the effects of desmin deletion on skeletal muscle at the transcriptional level across many pathways of muscle physiology. RNA was isolated from the TA muscle of mice of two genotypes (wildtype (WT) and desmin knockout (KO)) and two ages (7-9 weeks (Adult) and 12-14 months (Aged)). Numbers per group are as follows: WT_Adult (5), WT_Aged (5), KO_Adult (5), KO_Aged (4).
2012-07-10 | E-GEOD-34388 | biostudies-arrayexpress
Project description:Full title: Eccentric exercise activates novel transcriptional regulation of hypertrophic signaling pathways not affected by hormone changes. Unaccustomed eccentric exercise damages muscle tissue stimulating mechanisms of recovery and remodeling that may be affected by cellular protection by the sex hormone 17β-estradiol (E2). Using cDNA microarrays, we screened for differences in mRNA expression caused by E2 and eccentric exercise. After randomly assignment to 8 days of either placebo (CON) or E2 (EXP), eighteen men performed 150 single-leg eccentric contractions. Muscle biopsies were collected at baseline (BL), following supplementation (PS), +3 hours (3H) and +48 hours (48H) after exercise. Serum E2 concentrations increased significantly with supplementation (P < 0.001) but did not affect microarray results. Exercise led to early transcriptional changes in striated muscle activator of Rho signaling (STARS), Rho family GTPase 3 (RND3), mitogen activated protein kinase (MAPK) regulation and the downstream transcription factor FOS. Targeted RT-PCR analysis identified concurrent induction of negative regulators of calcineurin signaling RCAN (P < 0.001) and HMOX1 (P = 0.009). Protein contents were elevated for RND3 at 3H (P = 0.02) and FOS at 48H (P < 0.05). These findings indicate that early RhoA and NFAT signaling and regulation are altered following exercise for muscle remodeling and repair, but are not affected by E2.
2009-12-16 | GSE19062 | GEO
Project description:Eccentric exercise (ECC) can result in ultra-structural and histological damage to skeletal muscle. The damage incurred following ECC is typically followed by a subsequent regenerative and adaptive response. The specific mechanisms that drive this response, particularly in human muscle, are not well understood. The objective of this study was to characterize the early molecular response in skeletal muscle following ECC in humans. We used an Agilent whole human genome microarray to assess global gene expression in male subjects (N=35) at 3 hours post-100 eccentric contractions of the knee extensors. ANCOVA (age and BMI covariates) was used to compare mRNA expression between the ECC and non-exercised (CON) legs of each subject. Novel transcripts from IPA identified networks were confirmed with quantitative real-time (qRT)-PCR. qRT-PCR analysis of 3 of these transcripts (IkBα, TNFRSF1A and ICAM-1) confirmed changes observed in the microarray analysis. 35 male subjects performed an eccentric exercise protocol consisting of 100 maximal eccentric contrations of the knee extensors. 3 hours after the completion of the exercise regimen, a muscle biopsy was taken from the vastus lateralis of both legs. The non-exercised leg served as the control. Gene expresssion was analyzed using an ANCOVA, with covariates for age and BMI.
2010-10-04 | E-GEOD-23697 | biostudies-arrayexpress
Project description:Myofibrillar myopathy (MFM) in horses is a late onset disease that affects performance and athleticism. It is characterized by myofibrillar disarray and protein aggregation with no known cause. The objective of this study was to elucidate the molecular drivers of MFM in Warmblood (WB) horses by proteomic profiling (5 MFM WB, 4 non-MFM WB) of gluteal muscle. MFM horses used in this study had a chronic history of poor performance and exercise intolerance as well as accumulation of desmin aggregates in > 4 myofibers per muscle sample. The Equine Neuromuscular Diagnostic Laboratory database at Michigan State University was queried to identify WB horses with snap frozen gluteus medius biopsies available for analysis. Non-MFM control horses were defined as horses with no history of exercise intolerance and no evidence of desmin accumulation or other histopathology in muscle biopsies. Muscle biopsy samples were obtained at rest from horses that had not undertaken strenuous exercise in the preceding 48 hours.
2021-09-09 | PXD019187 | Pride
Project description:Skeletal muscle has an impressive ability to repair itself after a damaging insult and this response is essential to the process of muscle adaptation. In conditions such as muscular dystrophy and the sarcopenia of old age, repair is compromised leading to fibrosis and fatty tissue accumulation. Hypoxia-inducible factors (HIFs) are highly conserved regulators of gene transcription under conditions of low oxygen tension and HIF target genes such as EPO and VEGF have been associated with muscle protection and repair. We sought to interrogate the importance of HIF activation to skeletal muscle repair through the use of prolyl hydroxylase inhibitors (PHI) that stabilize HIF and activate target gene transcription in a mouse eccentric exercise limb damage model. We used microarrays to detail the global effects of prolyl hydroxylase inhibitors (PHI) in a mouse eccentric exercise limb damage model.
2017-08-23 | GSE95244 | GEO
Project description:We examined global mRNA expression using cDNA microarrays in skeletal muscle of humans before, and 3h and 48h after 300 maximal eccentric contractions. Keywords: Time course Healthy, non-trained university-aged subjects performed 300 single leg maximal eccentric contractions. Skeletal muscle biopsies were taken from the vastus lateralis before, 3h and 48h after the exercise bout. Total RNA was extracted, amplified, reverse transcribed, and cDNA was analyzed on a custom made cDNA microarray. Four subjects were analyzed, and samples were not pooled between subjects (i.e. individual microarrays were used for baseline vs. 3H and baseline vs. 48h for EACH subject; repeated measures design).
2006-04-15 | E-GEOD-4249 | biostudies-arrayexpress
Project description:Desmin, the major intermediate filament (IF) protein in muscle cells, interlinks neighboring myofibrils and connects the whole myofibrillar apparatus to myonuclei, mitochondria, and the sarcolemma. However, desmin is also known to be enriched at postsynaptic membranes of neuromuscular junctions (NMJs). The pivotal role of the desmin IF cytoskeletal network is underscored by the fact that over 100 mutations of the human DES gene cause hereditary and sporadic myopathies and cardiomyopathies. A subgroup of human desminopathies comprises autosomal recessive cases resulting in complete abolition of desmin protein. In these patients, who display a more severe phenotype than the autosomal dominant cases, it has been reported that some individuals also suffer from a myasthenic syndrome in addition to the classical occurrence of myopathy and cardiomyopathy. Since further studies on the NMJ pathology is hampered by the lack of available human striated muscle biopsy specimens, we exploited homozygous desmin knock-out mice which closely mirror the striated muscle pathology of human patients lacking desmin protein. Here, we report on the impact of the lack of desmin on the structure and function of NMJs and on the transcription of genes coding for postsynaptic proteins. Desmin knock-out mice display a fragmentation of NMJs in soleus, but not in extensor digitorum longus muscle. Moreover, soleus muscle fibers show larger NMJs. Further, transcription levels of acetylcholine receptor (AChR) genes are increased in muscles from desmin knock-out mice, especially of the AChR subunit, which is known as a marker of muscle fiber regeneration. Electrophysiological recordings depicted a pathological decrement of nerve-dependent endplate potentials and a faster rise time of the nerve-independent miniature endplate potentials. The latter is indicating an enhanced opening time of the AChR channels. Our study highlights the essential role of desmin for the structural and functional integrity of mammalian neuromuscular junctions.
2020-07-17 | GSE154573 | GEO
Project description:cDNA microarray analysis of human skeletal muscle after eccentric exercise
| PRJNA104621 | ENA