E-MEXP-703
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-703 | ExpressionAtlas | 2015-11-02
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:To study the effect of Sidt2 protein deficiency on skeletal muscle, we developed skeletal musclespecific Sidt2 gene knockout mouse model using Cre under the control of the MCK promoter We used microarrays to detail the changes of gene expression.
2018-04-17 | GSE113167 | GEO
Project description:We analyzed the functional role of DOR (Diabetes and Obesity Regulated gene) (also named Tp53inp2) in skeletal muscle. We show that DOR has a direct impact on skeletal muscle mass in vivo. Thus, using different transgenic mouse models, we demonstrate that while muscle-specific DOR gain-of-function results in reduced muscle mass, loss-of-function causes muscle hypertrophy. DOR has been described as a protein with two different functions, i.e., a nuclear coactivator and an autophagy regulator (Baumgartner et. al., PLoS One, 2007; Francis et. al., Curr Biol, 2010; Mauvezin et. al., EMBO Rep, 2010; Nowak et. al., Mol Biol Cell, 2009). This is why we decided to analyze which of these two functions could explain the phenotype observed in our mice models. In this regard, we performed a transcriptomic analysis using microarrays looking for genes differentially expressed in the quadriceps muscle of WT and SKM-Tg mice as well as in C and SKM-KO animals. Surprisingly, only a reduced number of genes were dysregulated upon DOR manipulation and most of the genes underwent mild changes in expression. These data strongly suggest that DOR does not operate as a nuclear co-factor in mouse skeletal muscle under the conditions subjected to study. In contrast, DOR enhances basal autophagy in skeletal muscle and promotes muscle wasting when autophagy is a contributor to muscle loss. To determine the functional role of DOR in skeletal muscle, we generated transgenic mice (SKM-Tg) overexpressing DOR specifically in skeletal muscle under the Myosin-Light Chain 1 promoter/enhancer. The open reading frame of DOR was introduced in an EcoRI site in the MDAF2 vector, which contains a 1.5 kb fragment of the MLC1 promoter and 0.9 kb fragment of the MLC1/3 gene containing a 3' muscle enhancer element (Rosenthal et. al., PNAS, 1989; Otaegui et. al., FASEB J, 2003). The fragment obtained after the digestion of this construct with BssHII was the one used to generate both transgenic mouse lines. Nontransgenic littermates were used as controls for the transgenic animals (Wt). In addition, a muscle-specific DOR knock-out mouse line (SKM-KO) was also generated by crossing homozygous DOR loxP/loxP mice with a mouse strain expressing Cre recombinase under the control of the Myosin-Light Chain 1 promoter (Bothe et. al., Genesis, 2000). Deletion of exons 3 and 4 driven by Cre recombinase caused the ablation of DOR expression. Non-expressing Cre DOR loxP/loxP littermates were used as controls for knockout animals (C). Four-month-old male mice were used in all experiments. Mice were in a C57BL/6J pure genetic background. We used microarrays to analyze the effect of DOR gain-of-function and DOR ablation on skeletal muscle gene expression Total RNA from quadriceps muscles from 4-month-old male mice was extracted and used for hibridization on Affimetrix microarrays
2014-02-13 | E-GEOD-54917 | biostudies-arrayexpress
Project description:Reversible epsilon-amino acetylation of lysine residues regulates transcription as well as metabolic flux; however, roles for specific lysine acetyltransferases in skeletal muscle physiology and function remain enigmatic. In this study, we investigated the role of the homologous acetyltransferases p300 and CBP in skeletal muscle transcriptional homeostasis and physiology in adult mice. Mice with skeletal muscle-specific and inducible knockout of p300 and/or CBP were generated by crossing mice with a tamoxifen-inducible Cre recombinase expressed under the human alpha-skeletal actin (HSA) promoter with mice harboring LoxP sites flanking exon 9 of both the Ep300 and Crebbp genes. Knockout was induced at 13-15 weeks of age via oral gavage of tamoxifen. We demonstrate that loss of both p300 and CBP in adult mouse skeletal muscle severely impairs contractile function and results in lethality within one week – a phenotype that is reversed by the presence of a single allele of either p300 or CBP. The loss of muscle function in p300/CBP double knockout mice is paralleled by substantial transcriptional alterations in gene networks central to skeletal muscle contraction and structural integrity. Changes in protein expression patterns, determined by 10-plex TMT labeling, were linked to impaired muscle function also manifest within days (WT mice were compared to day 3 and day 5 knock out mice). Together, these data reveal the requirement of p300 and CBP for the control and maintenance of contractile function and transcriptional homeostasis in skeletal muscle, and ultimately, organism survival. By extension, modulating p300/CBP function holds promise for the treatment of disorders characterized by impaired contractile function in humans.
2020-04-03 | PXD015694 | Pride
Project description:We analyzed the functional role of DOR (Diabetes and Obesity Regulated gene) (also named Tp53inp2) in skeletal muscle. We show that DOR has a direct impact on skeletal muscle mass in vivo. Thus, using different transgenic mouse models, we demonstrate that while muscle-specific DOR gain-of-function results in reduced muscle mass, loss-of-function causes muscle hypertrophy. DOR has been described as a protein with two different functions, i.e., a nuclear coactivator and an autophagy regulator (Baumgartner et. al., PLoS One, 2007; Francis et. al., Curr Biol, 2010; Mauvezin et. al., EMBO Rep, 2010; Nowak et. al., Mol Biol Cell, 2009). This is why we decided to analyze which of these two functions could explain the phenotype observed in our mice models. In this regard, we performed a transcriptomic analysis using microarrays looking for genes differentially expressed in the quadriceps muscle of WT and SKM-Tg mice as well as in C and SKM-KO animals. Surprisingly, only a reduced number of genes were dysregulated upon DOR manipulation and most of the genes underwent mild changes in expression. These data strongly suggest that DOR does not operate as a nuclear co-factor in mouse skeletal muscle under the conditions subjected to study. In contrast, DOR enhances basal autophagy in skeletal muscle and promotes muscle wasting when autophagy is a contributor to muscle loss. To determine the functional role of DOR in skeletal muscle, we generated transgenic mice (SKM-Tg) overexpressing DOR specifically in skeletal muscle under the Myosin-Light Chain 1 promoter/enhancer. The open reading frame of DOR was introduced in an EcoRI site in the MDAF2 vector, which contains a 1.5 kb fragment of the MLC1 promoter and 0.9 kb fragment of the MLC1/3 gene containing a 3' muscle enhancer element (Rosenthal et. al., PNAS, 1989; Otaegui et. al., FASEB J, 2003). The fragment obtained after the digestion of this construct with BssHII was the one used to generate both transgenic mouse lines. Nontransgenic littermates were used as controls for the transgenic animals (Wt). In addition, a muscle-specific DOR knock-out mouse line (SKM-KO) was also generated by crossing homozygous DOR loxP/loxP mice with a mouse strain expressing Cre recombinase under the control of the Myosin-Light Chain 1 promoter (Bothe et. al., Genesis, 2000). Deletion of exons 3 and 4 driven by Cre recombinase caused the ablation of DOR expression. Non-expressing Cre DOR loxP/loxP littermates were used as controls for knockout animals (C). Four-month-old male mice were used in all experiments. Mice were in a C57BL/6J pure genetic background.
2014-02-13 | GSE54917 | GEO
Project description:The aim of the experiment is to compare the effect of two different calcineurin A isoforms on skeletal muscle in uninjured mice and during skeletal muscle regeneration (after cardiotoxin injection). The transgenic mice express CnAbeta1 or CnAalpha under the control of the myosin light chain promoter and enhancer.
2007-12-31 | E-MEXP-703 | biostudies-arrayexpress
Project description:Different approaches of skeletal muscle cell regeneration originated from progenitor cells are extensively studied under the strategies of muscle tissue pathologies treatment. Recently it was discovered that anatomically localized alveolar mucosa multipotent mesenchymal stromal cells (AMC) are characterized by myogenic potential and high feasibility for muscle tissue recovery and regeneration. Although the resulting multinuclear myotubes are featured by expressing skeletal muscle specific markers (skeletal myosin, actin, myogenin and MyoD1) the exact molecular mechanism controlling differentiation of AMC in myogenic direction is still unclear and poorly scrutinized. In this research we used combination of large-scale transcriptome analysis and bioinformatics approach to appreciate molecular pathways and crucial nodes responsible for myogenic differentiation.
2019-07-13 | GSE134207 | GEO
Project description:Expression profiles of mouse skeletal muscle tissues, mouse skeletal muscle from Aged animals with high fat diet and chemical treatment
2019-07-16 | GSE134304 | GEO
Project description:Aged skeletal muscle is markedly affected by fatty muscle infiltration and strategies to reduce the occurrence of adipocytes within skeletal muscle, the intramuscular adipose tissue (IMAT), are urgently needed. Fibroblast growth factor-2 (FGF-2) is a critical growth factor for muscle tissue. Here, we show that FGF-2 not only stimulates muscle growth, but also promotes intramuscular adipogenesis. Using multiple screening assays for upstream and downstream signaling of microRNA (miR)-29a we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle from aged mice. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1 which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and AAV-mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular fat formation in vivo. Thus, our data highlight an ambivalent role of FGF-2 for adult skeletal muscle and reveal a novel pathway to combat fat accumulation in aged skeletal muscle.
2021-08-23 | PXD020575 | Pride
Project description:A commercially available gene array (SABiosciences array PAMM-029ZD-12) was used to assay gene expression in skeletal muscle of SMA mice and control littermates. The Taiwanese severe SMA mouse model was used (Hsieh-Li et al. 2000). The array included 84 genes associated with DNA damage detection, DNA repair, apoptosis, cell cycle, and other functions.
2014-03-03 | GSE55481 | GEO
Project description:Transgenic mice tagged with EGFP under the control of the endogenous Sox5, Sox6 and Sox9 promoter were used. E13.5 transgenic embryos were enriched for the skeletal elements and FACS was used to isolate the Sox5/6/9-expressing cells which were used for comparative expression profiling between wildtype and knockout.
2017-06-10 | GSE33173 | GEO