Role of Histone Deacetylase 4 on cardiac expression after exercise
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE72900 | GEO | 2017/06/07
SECONDARY ACCESSION(S): PRJNA295295
REPOSITORIES: GEO
Similar Datasets
Project description:Endurance exercise improves cardiac performance and affords protection against cardiovascular diseases but the signalling events that mediate these benefits are largely unexplored. Phosphorylation is an widely studied post-translational modification involved in intracellular signalling, and to discover novel phosphorylation events associated with exercise we have profiled the cardiac phosphoproteome response to a standardised exercise test to peak oxygen uptake (VO2peak). Male Wistar rats (346 ± 18 g) were assigned to 3 independent groups (n= 6, in each) that were familiarised with running on a motorised treadmill within a metabolic chamber. Animals performed a graded exercise test and were killed either immediately (0 h) after or 3 h after terminating the test at a standardised physiological end point (i.e. peak oxygen uptake; VO2peak). Control rats were killed at a similar time of day to the exercised animals, to minimise possible circadian effects. Cardiac proteins were digested with trypsin and phosphopeptides were enriched by selective binding to titanium dioxide (TiO2). Phosphopeptides were analysed by liquid chromatography and high-resolution tandem mass spectrometry, and phosphopeptides were quantified by MS1 intensities and identified against the UniProt knowledgebase using MaxQuant (v1.3.0.5). The VO2peak of rats in the 0 h and 3 h groups was 66 ± 5 ml•kg-1•min-1 and 69.8 ± 5 ml•kg-1•min-1, respectively. Proteome profiling detected 1169 phosphopeptides and one-way ANOVA found 141 significant (P<0.05 with a false discovery rate of 10 %) differences. Almost all (97 %) of the phosphosites that were responsive to exercise are annotated in the PhosphoSitePlus database but, importantly, the majority of these have not previously been associated with the cardiac response to exercise. More than two-thirds of the exercise-responsive phosphosites were different from those identified in previous phosphoproteome profiling of the cardiac response to β1-adrenergic receptor stimulation. Moreover, we report entirely new phosphorylation sites on 4 cardiac proteins, including S81 of muscle LIM protein, and identified 7 exercise-responsive kinases, including myofibrillar protein kinases such as obscurin, titin and the striated-muscle-specific serine/threonine kinase (SPEG) that may be worthwhile targets for future investigation.
2017-08-24 | PXD006646 | Pride
Project description:During acute sympathetic stress, the overeactivation of β-adrenergic receptors (β-ARs) caused cardiac fibrosis, by triggering inflammation and cytokine expression. It is unknown whether exercise training inhibited acute β-AR overactivation-induced cytokine expression and cardiac injury. Here, we reported that running exercise inhibited cardiac fibrosis and improved cardiac function in mice treated by isoproterenol, a β-AR agonist. Cytokine antibody array revealed that exercise prevented the expression changes of most cytokines induced by isoproterenol. Specifically, 18 ISO-upregulated and 3 ISO-downregulated cytokines belonged to six families (eg. chemokine) were prevented. A further KEGG analysis of these cytokines revealed that Hedgehog and Rap1 signaling pathways were involved in the regulation of cytokine expression by exercise. The expression changes of some cytokines that were prevented by exercise were verified by ELISA and real-time PCR. In conclusion, running exercise prevented the cytokine changes following acute β-AR overactivation and therefore attenuated cardiac fibrosis.
2019-03-30 | GSE129022 | GEO
Project description:Comparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy We performed microarray analysis on RNA from left ventricles of mice in non-pregnant diestrus cycle, mid-pregnancy (MP), late-pregnancy (LP), and immediate post-partum (0PP). These were compared to 7days (7EX) and 21 days (21EX) of voluntary wheel running exercise.
2012-03-08 | E-GEOD-36330 | biostudies-arrayexpress
Project description:Histone Deacetylase 4 (HDAC4) is known to contribute to cardiac remodeling processes. We wanted to identify and compare different genome wide targets of HDAC4 to well described interaction partners and its functional consequences. Therefore, we used a model of adult cardiomyocytes isolated from HDAC4 knockout mice and Wildtyp (WT) controls. We looked for HDAC4s contribution to changes of activating histone modifications (H3K4me3, H3K9ac, H3K27ac) and repressive pendants (H3K9me2 and H3K27me3).
2021-09-15 | E-MTAB-7319 | biostudies-arrayexpress
Project description:Gene expression data at rest and immediately post 30 min submaximal exercise in 3 month and 16 month old male rats, some of which were sedentary (SED), had access to a physical activity box twice weekly (PA) and some of which had daily access to a running wheel (EX). We used microarrays to detail global gene expression underlying select health-related phenotypes and identified differentially expressed genes among the three groups. Young (3 month) and old (16 month) male rats were separated into three different groups: Sedentary (SED), twice-weekly physical activity (PA), and regular exercise (EX). Animals were sacrificed either at rest or after 30 min of sub maximal exercise. Then, a portion of cardiac tissue was collected for RNA extraction and hybridization on Affymetrix microarrays.
2013-10-18 | E-GEOD-51380 | 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 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:Gene expression and phenotypic consequences of laboratory housing in rats. Disease related-phenotypes and associated gene expressions of sedentary animals (living solely in a standard cage) were compared with animals that had access to twice-weekly one-hour physical activity in a large box (PA) and with those that had access to voluntary running wheel exercise (EX). Keywords: exercise dose reponse, sedentary, twice weekly physical activity, daily exercise
2006-07-01 | GSE5085 | GEO
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:n total, 16 7-week-old male F344 rats were subjected to model regular exercise and sedentary lifestyle. In the second week after arrival and acclimatization to the reversed light/dark cycle, rats were introduced to the forced running wheel without a specific running mode. It was followed by a 12-day training phase for all 16 experimental animals (started at 9 weeks of age) by gradually increasing the running speed and duration. During the training phase, 8 best performers were selected for the runner group while the remaining 8 rats were assigned to the sedentary group. The regular forced running exercise phase for the runner group lasted for 5 weeks in total, including 4 weeks of regular running. After 4 weeks of regular exercise, rats underwent brief anesthesia and of blood from the tail vein were taken. This step was repeated for the same animals immediately after 1h of running. On the same day, a blood sample was collected from the sedentary rats following the same protocol. Plasma was collected and immediately frozen for further EV isolation. EVs were isolated from rat plasma by size exclusion chromatography. RNA libraries were constructed using CleanTag® Small RNA Library Prep Kit (Trilink Biotechnologies, USA) and sequenced on Illumina NextSeq500 instrument using NextSeq 500/550 Mid Output Kit v2.5 (150 cycles).
2021-12-28 | E-MTAB-11020 | biostudies-arrayexpress
Project description:Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome. Methods:; Soleus gene expression of both sedentary and exercise trained HCR and LCR was characterized by microarray- and gene ontology analysis. Results: Although HCR and LCR had an inborn 347% difference in running capacity, only three genes were found differentially expressed in the soleus muscle between the two groups. Up-regulation of the mitochondrial enzyme leucyl-transferRNA synthetase (LARS2) was found in the sedentary LCR. Increased expression of LARS2 has been associated with a mitochondrial DNA mutation linked to maternally inherited diabetes and mitochondrial dysfunction. In line with our findings, a growing body of evidence suggests that LCR have compromised mitochondrial function. After exercise training, 58 genes were altered in the soleus muscle of HCR, in contrast to only one in the LCR group. This suggests that animals born with different levels of fitness respond different to the same type of exercise training. Adaptations to exercise in HCR seemed to be associated with increased lipid metabolism and fatty acid elongation in the mitochondria. Also, genes associated with the peroxisomes, seemed to be central in the adaptation to exercise. Conclusion: The results indicate that (i) LCR might have mitochondrial dysfunction, which may be a contributing factor of the low inborn aerobic capacity, (ii) animals born with different levels of fitness respond different to the same exercise program. Experiment Overall Design: There are 16 samples in this study.
2008-06-18 | E-GEOD-10527 | biostudies-arrayexpress