Molecular characterisation of muscle and spinal cord tissues from young, old and old exercised C57BL/6 wild type male mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE122116 | GEO | 2019/08/31
REPOSITORIES: GEO
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Project description:Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogeninâs role in adult skeletal muscle is unclear. We sought to determine myogeninâs function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we monitored blood glucose and lactate levels and performed histochemical analysis on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle. We used microarrays to detail the global program of gene expression underlying enhanced exercise endurance associated with myog-deletion and long-term exercise training. Mouse gastrocnemius muscles were selected after 6 months of myog-deletion and exercise training for RNA extraction and hybridization on Affymetrix microarrays. We chose 3 wild type and 3 myog-deleted mice that best represented the average of each larger group that was tested during our mouse exercise studies.
2010-06-08 | E-GEOD-22046 | biostudies-arrayexpress
Project description:Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogenin’s role in adult skeletal muscle is unclear. We sought to determine myogenin’s function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we monitored blood glucose and lactate levels and performed histochemical analysis on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle. We used microarrays to detail the global program of gene expression underlying enhanced exercise endurance associated with myog-deletion and long-term exercise training.
2010-05-29 | GSE22046 | GEO
Project description:Purpose: The goal of this study was to determine the gene expression changes that occur over 7 days in parralyzed muscle in response to isometric contraction elicited by electrical stimulation initiated 4 months after spinal cord injury and to compare such changes to those observed in a normal muscle subjected to overload. Methods: Electrical stimulation of the soleus and plantaris muscle was stimulated in female rats with complete transection of the spinal cord at the interspace between the 9th and 10th thoracic vertebrae. Stimulation was begun 16 weeks after spinal cord transection and produced near-isometric contraction of soleus, plantaris and tibialis anterior. Muscle was analyzed at 1, 2 and 7 days after starting exercise with electrical stimulation. To provide a baseline reference for gene expression at 16 weeks after spinal cord injury, muscle was also analysed from an additional group of spinal cord transected animals. One additional group of animals with a sham-spinal cord injury was included to provide information about gene expression in neurologically intact animals of similar age. In parallel studies, rats underwent bilateral gastrocnemius ablation to overload soleus and plantaris, or a sham ablation as a control. Muscle was analyzed at 1, 3 and 7 days after gastrocnemius ablation or sham-ablation. Gene expression was determined using Affymetrix Rat Exon microarrays. For each group of animals, microarray analysis was performed for soleus muscle for each of 3 separate animals, using one array per animal. Control sammples for the spinal cord injured groups included a group of animals with a Sham-spinal cord injury, and a group of spinal cord injured animals that did not get electrical stimulation. The comparator for determining fold-change expression values was the spinal cord injured group that did not receive electrical stimulation. For each day after gastrocnemius ablation, a control was included that received all procedures needed for this ablation except cutting the distal insertion of the gastrocnemius into the Achilles tendon to control for effects of the surgery on gene expression.
2013-03-30 | E-GEOD-37476 | biostudies-arrayexpress
Project description:To address whether, after depletion by Csf1r inhibition, microglia repopulating the CNS revert to a “younger” phenotype, we treated a group of 23 months old mice with the Csf1r inhibitor for 5 days and let microglia repopulate the central nervous system for 7 days. Young (3 months old) and old (23 months old) mice were included as controls. After the repopulation time, whole spinal cord samples and Fluorescence Activated Sorting (FACS)-sorted microglia cells from brain tissue were collected to perform bulk transcriptome (RNAseq) analysis. Analysis of whole spinal cord suggested that repopulating microglia tend to re-acquire its original aged phenotype. Gene expression in FACS-sorted microglia was then analyzed to better characterize its intrinsic phenotype after repopulation. In contrast to the whole spinal cord samples, old and old-treated replicates separated in Principal Component Analysis, suggesting that repopulating microglia displayed a different phenotype compared to old microglia.
2019-08-31 | GSE122085 | GEO
Project description:This analysis was done to determine which muscle group has the most skeletal muscle transcriptional reponses to wheel running activity. Seven male mice with C57BL/6 genetic background were placed individually in cages with running wheels and allowed free access to the wheels 24 hr per day. Access to running wheels began when the mice were 6 months old, and continued for 12 weeks. The morning after the night of running, the mice were euthanized and several muscle groups were snap froze in liquid nitrogen to preserve RNA. The same muscle groups were collected from three age-matched "sedentary" mice that were housed in ordinary cages that did not permit sustained running. For each muscle group, separate pools of polyadenylated RNA from the sedentary and wheel-running mice were prepared for deep sequencing of cDNA with the SOLiD 3 platform.
2011-09-03 | GSE31843 | GEO
Project description:This analysis was done to determine which muscle group has the most skeletal muscle transcriptional reponses to wheel running activity. Seven male mice with C57BL/6 genetic background were placed individually in cages with running wheels and allowed free access to the wheels 24 hr per day. Access to running wheels began when the mice were 6 months old, and continued for 12 weeks. The morning after the night of running, the mice were euthanized and several muscle groups were snap froze in liquid nitrogen to preserve RNA. The same muscle groups were collected from three age-matched "sedentary" mice that were housed in ordinary cages that did not permit sustained running. For each muscle group, separate pools of polyadenylated RNA from the sedentary and wheel-running mice were prepared for deep sequencing of cDNA with the SOLiD 3 platform. Four muscle groups were examined (quadriceps femoris; gastrocnemius/plantaris; tibialis anterior; triceps brachii). For each muscle, RNA was pooled from 3 sedentary or 7 wheel-running mice (8 pools total).
2011-09-03 | E-GEOD-31843 | biostudies-arrayexpress
Project description:Four healthy human volunteers underwent an acute bout of resistance exercise with the right leg at 2 pm. Biopsies were removed from the Vastus Lateralis muscle 6 h (8 pm) and 18 h (8 am) after exericise
2007-08-21 | E-GEOD-1832 | biostudies-arrayexpress
Project description:Untargeted lipidomics of brain and spinal cord samples from female mice at 4, 12, 25, 48, and 78 weeks of age
2022-08-22 | MSV000090179 | GNPS
Project description:Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training. Keywords: resistance exercise, muscle, aging
2007-07-16 | GSE8479 | GEO
Project description:Analysis of skeletal muscle from taurine transporter (TauT) knockout mice at 3 or 18 months of age. Knocking out TauT result in a decrease in muscle cell size, impaired exercise capacity and accelerated muscle aging. Results provide molecular insights into physiological role of taurine.
2014-05-08 | GSE57373 | GEO