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Influence of low and high force muscle activity on paralyzed muscle gene expression

ABSTRACT: We used a novel approach to study the acute effect of two frequencies of stimulation (20 Hz and 5 Hz; high and low force, respectively) on gene regulation in people with chronic paralysis. Three hours after the completion of the electrical stimulation protocol (5 Hz or 20 Hz), we sampled the vastus lateralis muscle and examined genes involved with metabolic transcription, glycolysis, oxidative phosphorylation, and mitochondria remodelling. We discovered that the 5 Hz stimulation, despite generating a lower overall force, induced a 5-6 fold increase (p<0.05) in key metabolic transcription factors including PGC-1?, NR4A3, and ABRA. Neither protocol showed a robust regulation of genes for glycolysis, oxidative phosphorylation, and mitochondria remodelling. We analyzed skeletal muscle using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Partek Genomic Suites.

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Shields

PROVIDER: E-GEOD-64683 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Low-frequency stimulation regulates metabolic gene expression in paralyzed muscle.

Petrie Michael M Suneja Manish M Shields Richard K RK

Journal of applied physiology (Bethesda, Md. : 1985) 20150129 6

The altered metabolic state after a spinal cord injury compromises systemic glucose regulation. Skeletal muscle atrophies and transforms into fast, glycolytic, and insulin-resistant tissue. Osteoporosis is common after spinal cord injury and limits the ability to exercise paralyzed muscle. We used a novel approach to study the acute effect of two frequencies of stimulation (20 and 5 Hz) on muscle fatigue and gene regulation in people with chronic paralysis. Twelve subjects with chronic (>1 yr) a ...[more]

PMID: 25635001

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Influence of low and high force muscle activity on paralyzed muscle gene expression

Project description:We used a novel approach to study the acute effect of two frequencies of stimulation (20 Hz and 5 Hz; high and low force, respectively) on gene regulation in people with chronic paralysis. Three hours after the completion of the electrical stimulation protocol (5 Hz or 20 Hz), we sampled the vastus lateralis muscle and examined genes involved with metabolic transcription, glycolysis, oxidative phosphorylation, and mitochondria remodelling. We discovered that the 5 Hz stimulation, despite generating a lower overall force, induced a 5-6 fold increase (p<0.05) in key metabolic transcription factors including PGC-1α, NR4A3, and ABRA. Neither protocol showed a robust regulation of genes for glycolysis, oxidative phosphorylation, and mitochondria remodelling.

2015-08-01 | GSE64683 | GEO

Influence of muscle activity on paralyzed muscle

Project description:We investigated the short and long term effects of electrically induced exercise on mRNA expression of human paralyzed muscle. We developed an exercise dose that activated the muscle for 0.6% of the day. The short term effects were assessed 3 hours after a single dose of exercise, while the long term effects were assessed after training 5 days per week for at least one year (adherence 81%). A single dose of electrical stimulation increased the mRNA expression of transcriptional, translational, and enzyme regulators of metabolism important to shift muscle toward an oxidative phenotype (PGC-1a, NR4A3, IFRD1, ABRA, PDK4). However, chronic training increased the mRNA expression of specific metabolic pathway genes (BRP44, BRP44L, SDHB, ACADVL), mitochondrial fission and fusion genes (MFF, MFN1, MFN2), and slow muscle fiber genes (MYH6, MYH7, MYL3, MYL2).Furthermore, regulating these same pathways may be critical to developing efficient activity protocols to reduce the prevalence of diabetes in people with longstanding paralysis from SCI. We analyzed skeletal muscle using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Partek Genomic Suites.

2015-09-01 | E-GEOD-63423 | biostudies-arrayexpress

Cell of origin strongly influences genetic selection in a mouse model of T-ALL.

Project description:Thymic lymphomas were generated by inducing Sleeping Beauty transposon mutagenesis at different stages of T-cell development. This dataset includes exon array results from 14 tumor samples from two different Sleeping Beauty models of T-ALL (7 Vav-SB and 7 CD4-SB samples).

2011-08-20 | E-GEOD-29849 | biostudies-arrayexpress

Effect of fasting on human skeletal muscle mRNA levels

Project description:The goal of these studies was to determine the effects of fasting on skeletal muscle mRNA levels in healthy human subjects. Seven healthy adult human subjects fasted for 40 hours and then a muscle biopsy (fasting sample) was obtained from the vastus lateralis muscle. Immediately after the first muscle biospy, subjects then ate a mixed meal. Six hours after the first muscle biopsy, a second muscle biopsy (fed sample) was obtained from the contralateral vastus lateralis muscle. In each subject, mRNA levels under fasting conditions were normalized to mRNA levels under fed conditions, which were set at 1.

2011-06-08 | E-GEOD-28016 | biostudies-arrayexpress

Effect of ATF4 gene knockout on skeletal muscle mRNA levels in fasted mice.

Project description:ATF4 is a fasting-induced trascription factor that promotes skeletal muscle atrophy. The goal of these studies was to determine how of loss of ATF4 affects skeletal muscle mRNA expression. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls were fasted for 24 hours and then tibialis anterior muscles were harvested. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.

2012-09-15 | E-GEOD-39193 | biostudies-arrayexpress

Effect of denervation on mouse skeletal muscle mRNA levels.

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2012-09-15 | E-GEOD-39195 | biostudies-arrayexpress

Effect of ATF4 overexpression on mRNA levels in differentiated C2C12 myotubes.

Project description:ATF4 is a bZIP transcription factor that that promotes skeletal muscle atrophy. The goal of these studies was to determine the effects of ATF4 overexpression on mRNA levels in differentiated C2C12 myotubes. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12,2012 C2C12 myotubes were infected with adenovirus co-expressing eGFP and ATF4-FLAG. Control myotubes were infected with adenovirus co-expressing eGFP and a transcriptionally inactive ATF4 construct (ATF4∆bZIP).

2012-09-15 | E-GEOD-39194 | biostudies-arrayexpress

Effect of Gadd45a overexpression on mouse skeletal muscle mRNA levels.

Project description:Gadd45a is a stress-induced protein that causes skeletal muscle atrophy. The goal of these studies was to determine the effects of Gadd45a overexpression on mRNA levels in mouse skeletal muscle. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Tibialis anterior (TA) muscles from muscle-specfic ATF4 knockout mice (ATF4 mKO) were transfected with either 20 mg empty plasmid (pcDNA3) (left TA) or 20 mg pCMV-FLAG-Gadd45a (right TA) and harvested 7 days later. mRNA levels in Gadd45a-transfected muscles were normalized to levels in control transfected muscles.

2012-09-15 | E-GEOD-39196 | biostudies-arrayexpress

Cigarette smoking alters mRNA expression in human alveolar macrophages

Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%. 4 never smokers and 4 active smokers were recruited for the study. After bronchoalveolar lavage and RNA isolation, gene expression was measured using Affymetrix Human Exon 1.0 ST arrays.

2012-10-02 | E-GEOD-34517 | biostudies-arrayexpress

Expression data from MTDH knockdown in the Hec50co endometrial cancer cell line

Project description:Understanding the molecular underpinnings of chemoresistance is vital to design therapies to restore chemosensitivity. In particular, metadherin (MTDH) has been demonstrated to have a critical role in chemoresistance. Over-expression of MTDH has recently been implicated in poor clinical outcome in breast cancer, neroblastoma, hepatocellular carcinoma and prostate cancer. In this present study, we focused on the therapeutic benefit of MTDH depletion to restore sensitivity to cell death mediated by a combinatorial therapy of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL), which promotes death of cancerous cells of the human reproductive tract, and histone deacetylase (HDAC) inhibitors, which have been shown to increase sensitivity of cancer cells to TRAIL-induced apoptosis. Our data indicate that depletion of MTDH in endometrial cancer cells results in sensitization of cells that were previously resistant to cell death mediated by combinatorial treatment with TRAIL and HDAC inhibitor LBH589. MTDH was found to be involved in G2/M checkpoint regulation in response to LBH589 alone or LBH589 in combination with TRAIL, suggesting that MTDH functions at the cell cycle checkpoint to accomplish resistance.Using microarray technology, we identified 57 downstream target genes of MTDH, including Calbindin 1 and Galectin 1, which may contribute to MTDH-mediated resistance to combinatorial TRAIL and HDAC inhibitor targeted therapy. Inhibition of PDK1,AKT phosphorylation and increase Bim expression and XIAP degradation may result in sensitivity to cell death induction in MTDH depleted Hec50co cells by TRAIL and LBH 589 combination treatment. These findings indicate that depletion of MTDH is a potentially novel avenue for effective cancer therapy. The microarray was performed on three biological triplicates as well as three experimental triplictes of stable knockdown and control cells. MTDH was knocked down using a shRNA.

2010-12-17 | E-GEOD-26134 | biostudies-arrayexpress

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