Physiologic cardiac hypertrophy
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE776 | GEO | 2003/10/24
SECONDARY ACCESSION(S): PRJNA87737
REPOSITORIES: GEO
Similar Datasets
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:Seventy two rats were randomized to twelve independent groups of rats (n = 6 in all groups) where half of the rats were chosen for training (treadmill exercise training 1.5 hour 5 days a week, in 1, 4, 24, 48 days and for 4 and 8 weeks) or sedentary (no training) as described in detail by Wisloff et al. (Intensity-controlled treadmill running in rats: VO(2 max) and cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H1301-10.) or Kemi et al.(Aerobic fitness is associated with cardiomyocyte contractile capacity and endothelial function in exercise training and detraining. Circulation. 2004 Jun 15;109(23):2897-904. Epub 2004 Jun 1.). The rats were scarified one hour after training (1, 4, 24 and 48 days) or 24 hours after training (4 and 8 weeks). Biopsies form left ventricle was taken form all rats and stored on -80°C for preparation of RNA. The same procedures were performed for the control/sedentary rats which were sacrificed at the same time as the exercised rats.
2006-11-10 | E-TABM-166 | biostudies-arrayexpress
Project description:Microarray of exercised (degenerated) rat supraspinatus versus non-exercised (normal) rats were subjected to exercise that consisted of running on a 10Ë decline at 17m/min for 1 hour per day, 5 days per week. This regimen equates to approximately 7500 strides per day. After four weeks of running, rats were sacrificed by CO2 inhalation and both supraspinatus tendons were collected. 12 non-exercised rats were used as controls.
2010-07-01 | E-GEOD-4575 | biostudies-arrayexpress
Project description:The effects of exercise training (ET) on the heart of aortic stenosis (AS) rats are controversial and the mechanisms involved in alterations induced by ET have been poorly clarified. In this study we analyzed the myocardial proteome to identify proteins modulated by moderate intensity aerobic ET in rats with chronic supravalvar AS. Wistar rats were divided into four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary aortic stenosis (AS-Sed), and exercised AS (AS-Ex). ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal-Wallis and Goodman tests. Results were discussed at a significance level of 5%. At the end of the experiment, AS-Ex rats had higher functional capacity, lower blood lactate concentration, and better cardiac structural and left ventricular functional parameters than the AS-Sed. Myocardial proteome analysis showed that AS-Sed had higher protein expressions related to the glycolytic pathway, oxidative stress, and inflammation, and lower protein expressions related to beta-oxidation than C-Sed. AS-Ex had higher expression of one protein related to mitochondrial biogenesis and lower protein expressions associated with oxidative stress and inflammation than AS-Sed. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. In conclusion, chronic pressure overload changes the expression of myocardial proteins that are mainly involved in lipid and glycolytic energy metabolism in rats. Moderate intensity aerobic training attenuates protein expressions related to oxidative stress and inflammation and increases protein expressions related to mitochondrial biogenesis. Protein changes are associated with improved functional capacity, cardiac remodeling and left ventricular function in aortic stenosis rats.
2024-02-29 | PXD040785 | Pride
Project description:This study aimed to examine if early life exercise could normalize the reduced heart mass we have previously observed in the adult hearts from growth restricted rats. We investigated the molecular pathways using microarray analysis to explain how endurance exercise in early life might be regulating the sustained increase in heart mass we have observed in these rats in adulthood. At 5 weeks of age, male WKY rats were allocated to one of the following exercise treatments: remained sedentary with post mortem (PM) at 9 or 24 weeks, early exercise training (from 5-9 weeks of age) with PM at 9 or 24 weeks, or later exercise training (from 20-24 weeks of age) with PM at 24 weeks (n=8 males/group). Exercise training involved treadmill running 5 days/ week for 4 weeks. Running duration progressively increased from 20 up to 60 minutes per day, with the treadmill speed set at 15 m/min for the first week and 20 m/min thereafter. At 9 or 24 weeks of age rats were killed with an intraperitoneal injection of Ilium Xylazil-20 (30 mg/kg) and Ketamine (225 mg/kg). The rats in the 9 week old early exercise and 24 week old later exercise groups were killed 72 hours following the last bout of treadmill running. Total RNA was obtained from the whole-hearts for analysis
2015-12-09 | GSE75781 | GEO
Project description:Microarrays were used for transcription profiling of skeletal muscle samples taken at birth, when the phenotype was not expressed, and 12 weeks of age from Callipyge and wild type sheep. The genes that underlie the expression of the phenotype rather than result from the fibre type change in the affected muscle have been identified. We used microarrays to detail the global programme of gene expression underlying the hypertrophy phenotype and identified distinct classes of regulated genes during this process. A working model that links the muscle hypertrophy phenotype with a core group of transcriptional coregulators is proposed. Experiment Overall Design: Gene expression analyses were performed primarily on longissimus dorsi skeletal muscle (LD) from Wild type (NN) and Callipyge (NCpat) sheep using Bovine Affymetrix GeneChip microarrays. Two developmental time-points were investigated in this study: newborn (within 5 days of birth; T0) and 11-12 weeks post-birth (T12). The muscle hypertrophy phenotype developed over the first 2-3 months and was associated with a significant change in muscle fibre type (Carpenter et al., 1996; Cockett et al., 1994; 1996; Kerth et al., 2003). One of the objectives of the gene expression analysis was to delineate between those genes that underlie the muscle hypertrophy in Callipyge sheep and those that result from the fibre type change in the affected muscle. To address this issue a comparison was undertaken of gene expression in wild type skeletal muscles with differing fibre type compositions to identify fibre type specific genes. These samples were taken from NN animals at T12. The three skeletal muscles used in this analysis were semimembranosis (SM), semitendinosis (ST) and longissimus dorsi (LD).
2008-11-07 | E-GEOD-5955 | biostudies-arrayexpress
Project description:Rats were trained to orally self-administer alcohol in a concurrent, two-lever, free-choice contingency using a modification of the sweet solution fading procedure (O'Dell et al., 2004; Roberts et al., 2000; Vendruscolo et al., 2012). Following acquisition of self-administration, rats were allowed to self-administer unsweetened alcohol (10%) for 4 weeks and were then assigned to two groups matched by levels of responding: one group (dependent group) was exposed to chronic, intermittent ethanol vapors for 4 weeks to induce dependence; the other group (nondependent group) was not exposed to ethanol vapor. After a month of vapor exposure, rats were again tested during acute withdrawal (6-8 hours after removal from the vapor chambers) until stable levels of alcohol intake were achieved. As expected, alcohol vapor-exposed rats self-administered significantly greater amounts of alcohol than control rats not exposed to alcohol vapor during acute withdrawal. Rats were sacrificed during protracted abstinence (3 weeks after the end of alcohol vapor exposure) along with age-matched alcohol naive rats.
2014-11-13 | GSE60966 | GEO
Project description:This study aimed to examine if early life exercise could normalize the reduced heart mass we have previously observed in the adult hearts from growth restricted rats. We investigated the molecular pathways using microarray analysis to explain how endurance exercise in early life might be regulating the sustained increase in heart mass we have observed in these rats in adulthood. At 5 weeks of age, male WKY rats were allocated to one of the following exercise treatments: remained sedentary with post mortem (PM) at 9 or 24 weeks, early exercise training (from 5-9 weeks of age) with PM at 9 or 24 weeks, or later exercise training (from 20-24 weeks of age) with PM at 24 weeks (n=8 males/group). Exercise training involved treadmill running 5 days/ week for 4 weeks. Running duration progressively increased from 20 up to 60 minutes per day, with the treadmill speed set at 15 m/min for the first week and 20 m/min thereafter. At 9 or 24 weeks of age rats were killed with an intraperitoneal injection of Ilium Xylazil-20 (30 mg/kg) and Ketamine (225 mg/kg). The rats in the 9 week old early exercise and 24 week old later exercise groups were killed 72 hours following the last bout of treadmill running. Total RNA was obtained from the whole-hearts for analysis Total RNA obtained from the hearts of WKY rats. Male offspring remained sedentary or underwent treadmill running from 5-9 weeks (early exercise) or 20-24 weeks of age (later exercise).
2015-12-09 | E-GEOD-75781 | biostudies-arrayexpress
Project description:Down syndrome (DS) is a neurodevelopmental disorder caused by an extra copy of human chromosome 21 (HSA21). People with Down syndrome have poor motor skills and speech, impaired adaptive behavior, and cognition deficits. (Carlesimo et al., 1997; Contestabile et al., 2010; Roizen and Patterson, 2003; Sherman et al., 2007; Vicari et al., 2000). At the brain anatomical level, DS is characterized by structural deficiencies in diverse regions. These deficits include hippocampal and cortical growth reduction, abnormal lamination and differentiation of neurons, decreased dendritic branching and spine density, and abnormal synaptic plasticity (Kazemi et al., 2016; Rachidi and Lopes, 2011). Even though the genetic cause of DS was discovered in 1959 (Megarbane et al., 2009), we still do not know the precise mechanisms by which triplication of HSA21 genes leads to neuroanatomical and neurobehavioral phenotypes in DS individuals. Moreover, a fundamental question in DS is to discover the impact of the triplication of chromosome 21 on the global expression regulation of non-triplicated genes (Letourneau et al., 2014) and how these profound changes at the genetic level translate to phenotypic changes in DS individuals. Finally, drug treatments targeting various putative molecular pathways are effective in rescuing cognition in DS animals. Nevertheless, while the preclinical studies performed in diverse mouse models of DS have reported improvement in cognitive deficits, the same drugs have failed to replicate all the good and promising effects when administered to people with DS during clinical trials (Rueda et al., 2020). Therefore, there is a notable need in strongly extending our understanding of DS in humans. Global gene expression analysis at the mRNA or protein level with different techniques have reported interesting findings on disparate DS-derived samples (fibroblasts, circulating immune cells, and amniocytes) (Guedj et al., 2016; Stamoulis et al., 2019; Waugh et al., 2019; Lanzillotta et al., 2020; Liu et al., 2017. Liu et al., 2018; Sommer et al., 2008) or iPSC-derived neurons obtained from DS individuals (Gonzales et al., 2018; Huo et al., 2018; Sobel et al., 2019). However, only a few studies have directly assessed global mRNA dysregulation in the adult DS brains by microarray hybridization (Lockstone et al., 2007; Olmos-Serrano et al., 2016). Although the latter studies have provided interesting information about the significant cellular pathways altered in trisomy, they lacked the depth, sensitivity, and isoform specificity that characterize modern gene expression analysis by next-generation sequencing (NGS). In this regard, another study used single-nucleus RNA sequencing (snRNA-seq) to profile aging DS brains (Palmer et al., 2021). Although this cutting-edge technique can deliver high-level information for the characterization of cellular diversity in brain tissues, this comes at the cost of profiling less number of genes (Bakken et al., 2018) and the possibility of missing the specific signature of important pathological processes (Thrupp et al., 2020). Moreover, none of these studies addressed the other side of the coin, assessing the corresponding changes in protein expression. In fact, the question of how well the transcriptome expression profiles match with those at the protein level remains largely unanswered. Large-scale analysis of transcriptome and proteome of the human brain would therefore provide a more comprehensive data-driven approach to identify dysregulated biological processes or genes/proteins co-expression networks as drivers of disease pathogenesis and prioritize the development of corresponding therapeutic interventions. Here, we took a multi-level data acquisition and interpretation approach to integrate in-depth transcriptomics and proteomics data in parallel from the same set of human brain samples to identify dysregulated expression networks in DS, a complex and multigenic neurodevelopmental disorder. We also provide unprecedented evidence of changes in mRNA transcript (isoform) expression, and to our knowledge, a first integrative analysis to identify alternative splicing, RNA binding proteins, and miRNAs as crucial intermediate regulatory steps in DS. Our data provide molecular information signatures that consistently repeat at gene, transcript, and protein levels and may function as critical players in DS pathophysiology. In particular, our multi-level data pinpoint to alteration in cell projection genes that translate into defects in axon and dendrites formation, which we find in DS iPSC derived neurons and primary hippocampal culture from a murine DS model.
2024-06-03 | PXD038791 | Pride
Project description:The adaptation of regimented exercise in skeletal muscle including muscular hypertrophy and enhanced strength decline significantly with aging. Transcriptome analysis following RNA sequencing reveals extensive activation of hypoxia-related genes in young exercised mice versus the sedentary, but absent in aged exercised mice. Particularly, less expression of aryl hydrocarbon receptor translocator (ARNT) was observed in response to exercise in aged mice. Young mice underwent skeletal muscle-specific knockout of ARNT (ARNT mKO) obtain deficient benefit from exercise resembling the aged mice. The deletion of ARNT associated with decreased expression of Notch1 intracellular domain(N1ICD) impair muscle hypertrophy and regeneration. Administration of ML228, a systematic agonist of ARNT, rescued skeletal muscle adaptabilities in old mice, which was suppressed by administrating N1ICD inhibitor(DAPT). These results suggest that the loss of skeletal muscle ARNT is partially responsible for diminished response to exercise in aging and activation of hypoxia signaling holds promise for rescuing the adaptability in aged muscle.
2021-12-31 | GSE155937 | GEO