Mus musculus
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ABSTRACT:
PROVIDER: PRJNA229772 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Involvement of miRNAs in the regulation of muscle wasting during catabolic conditions
| PRJNA224203 | ENA
Project description:Prolonged fasting-induced changes in rat tibialis anterior muscle transcriptome Skeletal muscle is of primary importance for metabolism, thermogenesis and locomotion. However, muscle integrity is inevitably challenged throughout life, and muscle atrophy occurs in various situations, being associated with development of metabolic diseases. There is virtually no fully effective countermeasure today to fight the loss of muscle mass. It is therfore needed to understand in depth how muscle mass is regulated in wasting conditions. The aim of this study was to decipher the transcriptional regulations involved in prolonged fasting-induced muscle wasting during the phase of protein sparing (P2) and the late phase of increased body protein mobilization (P3). The main findings show that gene expression changes reflect well the intense use of lipids as fuels during P2 and increased use of muscle proteins during P3. Changes in muscle transcriptome for downstream signaling of anabolic and catabolic hormones (Smad, NFKB, EiF2alpha-ATF4, autophagy, ubiquitin-proteasome, Foxo, AMPK, PI3K/AKT, and mTOR pathways) and for the response to oxidative stress, transcription and translation processes, and myogenesis are generally consistent with increased muscle protein degradation and repressed synthesis, in a more marked manner during P3 than P2 compared to the fed state. Nevertheless, several changes appeared to be in favour of muscle protein synthesis during fasting, notably at the level of PI3K/AKT and mTOR pathways, transcription and translations processes, and the response to oxidative stress. They could constitute mechanisms that promote protein sparing during P2 and anticipate refeeding during P3 for restoration of the protein compartment. Future studies should examine validity of such targets for improving nitrogen balance during catabolic diseases.
2020-10-02 | GSE149829 | GEO
Project description:Hypothalamic interleukin-1 beta (IL-1β) production is induced in multiple inflammatory diseases associated with muscle catabolism. To determine whether IL-1β signaling in the CNS plays a role in the muscle wasting of inflammatory disease, we examined the ability of intracerebroventricular (ICV) IL-1β injection at pathophysiologically relevant concentrations, to generate catabolic changes in skeletal muscle. Changes in gene expression associated with these catabolic changes were monitored using gene expression exon arrays. 28 samples were analyzed. The following comparisons were made: 6 groups were defined on the basis of treatment and time. Differences between groups were assesed by one way-ANOVA. P values were corrected for multiple comparisons using the Benjamini Hochberg correction at a false discovery rate of 1%. Probes were considered that showed a 1.75 fold or greater up or down regulation at any of the three timepoints.
2011-11-03 | E-GEOD-26766 | biostudies-arrayexpress
Project description:Forkhead BoxO (FoxO) transcription factors expressed in adult skeletal muscle promote muscle atrophy during various catabolic conditions. We have identified the genome wide target genes and biological networks regulated by FoxO in skeletal muscle during Colon-26 (C-26) cancer cachexia. In this dataset, we include the expression data obtained from the tibialis anterior muscles of control and severely cachectic Colon-26 mice in which FoxO-dependent transcription was either intact (AAV9-EV) or inhibited (AAV9-d.n.FoxO). These data were used to obtain 543 FoxO target genes during cancer. These target genes were identified as those genes whose expression was both differentially regulated in skeletal muscle in response to cancer (control AAV9-EV vs. C26 AAV9-EV), and differentially regulated in the presence of d.n.FoxO (C26 AAV9-EV vs. C26 AAV9-d.n.FoxO).
2014-12-31 | GSE56555 | GEO
Project description:Skeletal muscle wasting is a debilitating condition that occurs with aging and with many diseases, but the underlying mechanisms are incompletely understood. Previous work determined that common transcriptional changes occur in skeletal muscle during atrophy induced by different stimuli. However, whether this holds true at the proteome level remains largely unexplored. Here, we find that, contrary to this earlier model, distinct atrophic stimuli (corticosteroids, cancer, and aging) induce largely different mRNA and protein changes during muscle wasting in mice. Moreover, there is widespread transcriptome-proteome disconnect. Consequently, atrophy markers (atrogenes) identified in earlier microarray-based studies do not emerge from these proteomic surveys as the most relevantly associated with atrophy. Based on these analyses, we identify atrophy-regulated proteins (here defined as “atroproteins”) such as the myokine CCN1/Cyr61, which we find regulates myofiber type switching during sarcopenia. Altogether, these integrated analyses indicate that different catabolic stimuli induce muscle wasting via largely distinct mechanisms.
2021-10-22 | GSE159952 | GEO
Project description:Skeletal muscle in fish presents a high plasticity controlled by a dynamic balance between anabolic and catabolic signaling pathways. Decreased food availability can inhibit muscle growth and trigger muscle catabolism pathways, thu promoting muscle atrophy. In contrast, anabolism may be favored during restoration of food supply, promoting the muscle growth. Considering this, we analyzed fast-twitch muscle of juvenile Piaractus mesopotamicus (pacu) submitted to a prolonged fasting (30 days) and refeeding (up to 30 days) using shotgun proteomics and gene expression analysis. The relative rate of weight and length increase, as well as the expression of mafbx and igf -1 genes, suggest that prolonged fasting caused muscle atrophy and that 30 days of refeeding led to partial compensatory growth. Shotgun proteomics analysis identified 99 proteins after fasting and 71 proteins after refeeding periods, of which 23 and 17 were differentially expressed after fasting and after 30 days of refeeding, respectively. Most of these differentially expressed proteins were related to cytoskeleton, muscle contraction and muscle metabolism. Among these, parvalbumin (PVALB), a calcium-binding protein and food allergen, was selected for further RT-qPCR analysis, which showed that pvalb mRNA was not changed after 30 days of fasting and 30 days of refeeding, but it was downregulated after 6h and 24h of refeeding. This suggests a post-transcriptional regulation of PVALB in fish muscle. In conclusion, our results suggest that muscle atrophy and partial compensatory growth caused by prolonged fasting and refeeding affected the muscle proteome and PVALB expression. Our results can contribute to the understanding of muscle anabolic and catabolic pathways in response to changes in food availability.
2019-11-28 | PXD014232 | Pride
Project description:Cancer cachexia is a devastating metabolic syndrome characterized by systemic inflammation and massive muscle and adipose tissue wasting. Although cancer cachexia is responsible for approximately one third of cancer deaths, no effective therapies are available and the underlying mechanisms have not been fully elucidated.We have found that (+)-JQ1 administration protects tumor-bearing mice from body weight loss, muscle and adipose tissue wasting. Remarkably, in C26-tumor bearing mice (+)-JQ1 administration dramatically prolongs survival, without directly affecting tumor growth. By ChIP-seq analyses, we unveil that the BET proteins directly promote the muscle atrophy program during cachexia. Consistently, BET pharmacological blockade prevents the activation of catabolic genes associated with skeletal muscle atrophy and decreases IL6 systemic levels. Overall, these findings indicate that BET may represent a promising therapeutic target in the management of cancer cachexia.
2017-10-01 | GSE104155 | GEO
Project description:A limited mechanistic understanding of skeletal muscle wasting after acute spinal cord injury (SCI) precludes targeted molecular interventions. Here, we demonstrate marked systemic wasting also affecting neurologically intact non-paralyzed (supralesional) muscle early after SCI. Systemic muscle mass loss propagates muscle weakness, affects fast type 2 myofibers preferentially, and becomes exacerbated after high (T3) compared to low (T9) thoracic paraplegia indicating lesion-level dependent (“neurogenic”) mechanisms. The wasting of non-paralyzed muscle, its rapid onset and severity beyond what can be explained by disuse implies additional systemic drivers. Muscle transcriptome and biochemical analysis revealed a glucocorticoid-mediated catabolic signature of SCI-induced systemic muscle wasting that was mitigated i) by endogenous glucocorticoid ablation (adrenalectomy), ii) by pharmacological glucocorticoid receptor (GR) blockade, and was iii) completely prevented, relative to T9 SCI, by genetic muscle-specific GR deletion. We provide evidence of neurogenic hypercortisolism underlying a rapid systemic and functionally relevant muscle wasting syndrome after acute SCI.
2024-01-31 | GSE224186 | GEO
Project description:Differentially expressed genes during disuse atrophy.
| PRJNA174343 | ENA
Project description:Hypothalamic interleukin-1 beta (IL-1β) production is induced in multiple inflammatory diseases associated with muscle catabolism. To determine whether IL-1β signaling in the CNS plays a role in the muscle wasting of inflammatory disease, we examined the ability of intracerebroventricular (ICV) IL-1β injection at pathophysiologically relevant concentrations, to generate catabolic changes in skeletal muscle. Changes in gene expression associated with these catabolic changes were monitored using gene expression exon arrays.
2011-11-03 | GSE26766 | GEO