Transcription profiling of heart tissue from rats that have undergone treadmill exercise or have been sedentary for different lengths of time
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Vidar Beisvag
PROVIDER: E-TABM-166 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Consequence of physical exercise in skeletal muscle was investigated in C57BL/6 mice after 4 weeks of exercise training and compared to sedentary controls. Exercised mice received four 4 weeks of regular exercise training on a motorized treadmill and were compared to sedentary controls. 6 mice of each Treatment were used to extract RNA from the quadriceps muscle three hours after the last training bout
2015-02-01 | E-GEOD-54276 | 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
Project description:Endurance exercise training has been shown to decrease whole-body and skeletal muscle insulin resistance and increase glucose tolerance in conditions of both pre-diabetes and overt type 2 diabetes. However, the adaptive responses in skeletal muscle at the molecular and genetic level for these beneficial effects of exercise training have not been clearly established in an animal model of pre-diabetes. The present study identifies alterations in skeletal muscle gene expression that occur with exercise training in pre-diabetic, insulin-resistant obese Zucker (fa/fa) rats and insulin-sensitive lean Zucker (Fa/-) rats. Treadmill running for up to 4 weeks caused significant enhancements of glucose tolerance as assessed by the integrated area under the curve for glucose (AUCg) during an oral glucose tolerance test in both lean and obese animals. Using microarray analysis, a set of only 12 genes was identified as both significantly altered (>1.5-fold change relative to sedentary controls; p<0.05) and significantly correlated (p<0.05) with the AUCg. Two of these genes, peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a) and the z-isoform of protein kinase C (PKC-z), have known involvement in the regulation of skeletal muscle glucose transport. We confirmed that protein expression levels of PGC-1a and PKC-z were positively correlated with the mRNA expression levels for these two genes. Overall, this study has identified a limited number of genes in soleus muscle of lean and obese Zucker rats that are associated with decreased insulin resistance and increase glucose tolerance following endurance exercise training. These findings could guide the development of pharmaceutical M-^Sexercise mimeticsM-^T in the treatment of insulin-resistant, pre-diabetic or overtly type 2 diabetic individuals.
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Project description:Here we describe a genome-wide analysis of DNA-methylation in muscle of trained mice. In comparison to sedentary controls 2762 genes exhibited differentially methylated CpGs in their putative promoter regions. The majority of these genes were related to muscle growth and differentiation and a minor fraction involved in metabolic regulation. These findings suggest that DNA-methylation is involved in the regulation of muscle adaptation to regular exercise training. Reduced representation bisulfite sequencing of murine quadriceps muscle
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Project description:Dahl salt-sensitive (DS) rats were obtained from Harlan Sprague Dawley Laboratory at 5 weeks of age. At 6 weeks of age, physiologic cardiac hypertrophy was generated by a; vigorous daily exercise regimen for 6 weeks (e group). The exercise protocol is based on those described previously with modifications (Wisloff U et al., 2001; Jin H et al., 1994). Rats were exercised daily for 6 weeks on a rodent treadmill (Exer-6M; Columbus Instruments). The exercise program consisted of three weeks of progressively strenuous exercise regimens; followed by three weeks of maintenance period, during which the rats were exercised at 16 m/min at a 5o incline for 90 minutes/day. All rats completed the exercise protocol. Pathological cardiac hypertrophy was generated by feeding a 6% NaCl diet to DS rats at 6 weeks of age (h group) (Inoko M et al., 1994). Control rats (c group) were age matched and sedentary DS rats fed normal rat chow. Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/rat_home.html<br><br>Note that files GSM11886.txt and GSM12308.txt, and files GSM11887.txt and GSM12309.txt as downloaded from GEO contain identical data.
2007-10-11 | E-GEOD-776 | biostudies-arrayexpress
Project description:Physical exercise training is a known protective factor against cardiovascular morbidity and mortality. Nevertheless, the underlying specific molecular mechanisms still remain uncompletely explored. To identify molecular mechanisms by which exercise training induces this favorable phenotype a genomic approach was used in an animal model of mild exercise previously demonstrated by our group to induce cardioprotection. Our data indicate that mild exercise by inducing no or few permanent changes in gene expression profile is able to determine cardioprotection without induction of cardiac hypertrophy. Experiment Overall Design: We investigated the gene expression profile by Affymetrix technology (230 2.0 GeneChip rat genome array) induced by mild exercise training (treadmill running: 25 m/min, 10% incline, 1 h/day, 3 days/week, 10 weeks) on left ventricle (LV) of exercise-trained (n=10) and sedentary control (n=10) rats.
2008-04-09 | E-GEOD-7640 | biostudies-arrayexpress
Project description:While the salutary effects of exercise training on conduit artery endothelial cells have been reported in animals and humans with cardiovascular risk factors or disease, whether a healthy endothelium is alterable with exercise training is less certain. The purpose of this study was to evaluate the impact of exercise training on transcriptional profiles in normal endothelial cells using a genome-wide microarray analysis. Brachial and internal mammary endothelial gene expression was compared between a group of healthy pigs that exercise-trained for 16-20 weeks (n=8) and a group that remained sedentary (n=8). We found that a total of 130 genes were up regulated and 84 genes down regulated in brachial artery endothelial cells with exercise training. In contrast, a total of 113 genes were up regulated and 31 genes down regulated in internal mammary artery endothelial cells (>1.5-fold and false discovery rate<15%). Although there was an overlap of 66 genes (59 up regulated and 7 down regulated with exercise training) between the brachial and internal mammary arteries, the identified endothelial gene networks and biological processes influenced by exercise training were distinctly different between the brachial and internal mammary arteries. These data indicate that a healthy endothelium is indeed responsive to exercise training and support the concept that the influence of physical activity on endothelial gene expression is not homogenously distributed throughout the vasculature. Brachial and internal mammary endothelial gene expression was compared between a group of healthy pigs that exercise-trained for 16-20 weeks (n=8) and a group that remained sedentary (n=8). The arteries were taken from the same animals, and after quality assessment, so there were 29 total arrays (15 unique pigs), 14 with an array for both the brachial artery and the internal mammary artery (IMA), and the remaining 1 having only brachial. One pig had bad RNA quality and is missing from both IMA and brachical. Therefore, there were 15 IMA (7 SED, 8 EX) and 14 brachial arrays (7 SED, 7 EX) that were used in this study.
2011-12-02 | E-GEOD-26663 | biostudies-arrayexpress
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).
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Project description:Many studies have reported on beneficial aspects of running to improve hippocampus-related spatial memory and promote neuroplastic changes like adult hippocampal neurogenesis (AHN). Such research has also revealed molecular factors associated with molecular signaling by BDNF and IGF-I leading to CREB activation. However, the optimum exercise intensity for genome-wide beneficial effects remains unclear. We thus investigate the whole spectrum of hippocampal molecular change by exercise using DNA microarray-based transcript profiling in two different intensity groups. Lactate threshold (LT), at which lactate starts to accumulate in the blood, defined the intensity: mild- (ME, <LT) or intense-exercise (IE, >LT). Rats were subjected to 6 weeks of training or sedentary (CONT) regimes. After 6 weeks, spatial memory using Morris Water Maze (MWM), AHN, and hippocampal gene expressions were assessed. 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This study is the first step to identify the potential triggers of exercise-induced cognitive gain. Eleven-week-old male Wistar rats (220-270 g; SLC, Saitama, Japan) were housed in polycarbonate steel cages with a 12-h light/dark schedule (lights on at 7:00 a.m.) and given ad libitum access to food and water. A total of 98 rats were used in this study to assess the influence of exercise intensity on physiological states (training effect of skeletal muscle and stress level) (n= 22), MWM (n= 32), AHN (n= 22), and global gene expression profiles of hippocampal by microarray (n= 22). All animal care and experimental procedures were performed in accordance with protocols approved by the University of Tsukuba Animal Experiment Committee, based on the National Institute of Health (NIH) Guidelines for the Care and Use of Laboratory Animals (NIH publication, revised 1996). All efforts were made to minimize animal suffering and to reduce the number of animals used in this study. To adapt the rearing environment and remove any unintended stress effects, animals underwent a week of preliminary rearing to ambient conditions in groups housing conditions (2-3 rats/cage). After the preliminary rearing, the animals were randomized into three groups based on the LT of treadmill running: Sedentary control (CONT, rest on treadmill), Mild Exercise (ME, below LT, 15 m/min) or Intense Exercise (IE, above LT, 40 m/min). Exercise group was habituated to run on a treadmill (KN-73, Natsume Ltd., Tokyo, Japan) for 1 (for ME) or 4 (for IE) weeks. Within a given test period, rats were able to run on the above-mentioned running speeds. After this running habituation, rats were entered into the exercise training session for 6 weeks in total. The running duration was 60 min/day and frequency was 5 times/week. Exercise training was performed between 19:00 and 22:00 (during dark phase). Rat’s body weight and physical condition were monitored until the end of training. If rats could not perform well running on each determined speed and showed poor health, those were eliminated from the study. Based on the criteria, a total of 13 rats were eliminated (bad runner - 4 rats; poor health - 7 rats). Twenty-four or thirty-six hours after the last training, rats were processed to the next step. In the microarray group, the whole brain of each animal was rapidly removed, and hippocampus was separated on ice according to the method of Glowinski and Iversen (1966), with minor modifications. Hippocampi were immediately flash-frozen in liquid nitrogen. The deep-frozen hippocampi were transferred to a pre-chilled (in liquid nitrogen) mortar and pestle, and ground to a very fine powder with liquid nitrogen. The powdered samples were stored in aliquots at -80ºC till used for further analysis. Total RNA was extracted from each sample powder (~50 mg) using the QIAGEN RNeasy Mini Kit (QIAGEN, Maryland, USA). To verify the quality of this RNA, the yield and purity were determined spectrophotometrically (NanoPhotomaterTM, IMPLEN, Munich, Germany) and visually confirmed using formaldehyde gel electrophoresis. We used the sample with a ratio of spectrophotometric absorbance at 260 nm to that at 230 (A260/A230) or 280 nm (A260/A280) above 1.8. An equal amount of RNA (1000 ng) from the five rats, randomly picked up from each exercise group (n = 5), was pooled and used for microarray analysis. In this study, we performed three combinations of comparison analysis of gene expression change. First, we compared the difference between CONT and ME (combination 1) or IE (combination 2) to confirm the exercise-intensity-dependent gene expression change. Subsequently, we made a comparison of ME with IE (combination 3) to elucidate a ME-based difference of IE inducible gene. In all combinations, total RNA (1000 ng) was labeled with either Cy3 or Cy5 dye using an Agilent Low RNA Input Fluorescent Linear Amplification Kit (Agilent Technologies Inc., CA, USA). Fluorescently labeled targets of control as well as treated samples were hybridized to the same microarray slide with 60-mer probes (4 x 44K (41,090 gene probes), rat whole genome, Agilent). A flip labelling (dye-swap or reverse labelling with Cy3 and Cy5 dyes) procedure was followed to nullify the dye bias associated with unequal incorporation of the two Cy dyes into cDNA. Hybridization and wash processes were performed according to the manufacturer’s instructions, and hybridized microarrays were scanned using an Agilent Microarray scanner. For the detection of significantly differentially expressed genes between control and exercise samples each slide image was processed by Agilent Feature Extraction software (version 9.5.3.1).
2014-04-05 | E-GEOD-45813 | biostudies-arrayexpress