Expression data from mouse skeletal muscle
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE39009 | GEO | 2012/06/30
SECONDARY ACCESSION(S): PRJNA169612
REPOSITORIES: GEO
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Project description:We generated skeletal muscle-specific knockout mice lacking the transcription factor Yin Yang 1 (YY1) and analyzed expression patterns in the skeletal muscle these mice. We used microarrays to detail the global programme of gene expression regulated by YY1. Wild type or knockout mice at 6 months were sacrificed and the soleus was isolated for RNA extraction.
2012-06-29 | E-GEOD-39009 | biostudies-arrayexpress
Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list. Murine skeletal muscle cells (C2C12 cells) were differentiated for 0, 1 or 3 days. Total RNAs were isolated from the cells and used for array profiling of miRNA expression.
2011-12-31 | E-GEOD-32238 | biostudies-arrayexpress
Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list.
2011-12-31 | GSE32238 | GEO
Project description:Skeletal muscle satellite cells (SCs) are adult muscle stem cells responsible for muscle regeneration after acute or chronic injuries. The lineage progression of quiescent satellite cells toward activation, proliferation and differentiation during the regeneration is orchestrated by cascades of transcription factors (TFs). Here we elucidate the functional role of a ubiquitously expressed TF, Yin Yang1 (YY1) in muscle regeneration. Muscle-specific deletion of YY1 in embryonic muscle progenitors leads to severe deformity of diaphragm muscle formation thus postnatal death. Inducible deletion of YY1 in satellite cells almost completely blocks the acute damage induced muscle repair and exacerbates the chronic injury induced dystrophic phenotype. Examination of SCs revealed that YY1 loss results in cell autonomous defect in cell activation and proliferation. Mechanistic search through genome-wide profiling of YY1 regulated transcriptome and YY1 binding revealed that YY1 binds and suppresses mitochondrial gene expression. Simultaneously, it also activates Hif1α mediated glycolytic genes to facilitate a metabolic reprogramming toward glycolysis which is needed for SC activation. Altogether our findings have identified YY1 as a key regulator of SC metabolic reprogramming during cell activation through its dual roles in modulating both mitochondrial and glycolytic pathways.
2019-04-09 | GSE108249 | GEO
Project description:Evidence suggests that diabetes mellitus is a promoting factor of sarcopenia; mechanism of how diabetes mellitus accelerates the development of sarcopenia is not known. We have recently established a model of diabetes-induced skeletal muscle mass loss in mice by using streptozotocin. We used microarrays to detail the global programme of gene expression underlying skeletal muscle atrophy in STZ treated mice and identified up-regulated or down-regulated genes during this process.
2018-12-11 | GSE123540 | GEO
Project description:Adult skeletal muscle stem cells (MuSCs), also known as satellite cells (SCs), are widely believed to be responsible for muscle regeneration, which is regulated by complex networks of intrinsic and extrinsic factors. Emerging evidence demonstrates extrinsic regulations from other cell types can significantly impact the regeneration process, especially in repetitive cycles of degeneration/regeneration environment. Here, we demonstrate that the transcription factor (TF) Yin Yang 1 (YY1) deletion in MuSCs of mdx mouse induces CCL5 expression by alleviating the repressive effect on 3D structural interactions on Ccl5 locus. This leads to the increased secretion of CCL5 from MuSCs to the muscle niche, which promotes the recruitment of macrophages (MPs) through the CCL5/CCR5 axis. Incremental MPs lead to continuous inflammation that promotes the survival of Fibro-adipogenic progenitors’ (FAP) through secreting elevated TGFβ1 to stimulate FAPs resisting apoptosis, resulting in aggravated dystrophic pathology manifested by exacerbated fibrosis. Inhibition of CCL5/CCR5 axis by Maraviroc injection effectively mitigates muscle dystrophy and enhances muscle performance in YY1 deletion mdx mouse. Altogether, our findings promote us to conclude that YY1 functions as a 3D structural protein to repress Ccl5 production at the transcriptional level in MuSCs, playing a critical role in orchestrating MuSC/MP/FAP crosstalk through CCL5/CCR5 and TGFβ1 signaling. Intrinsic deletion of YY1 in MuSCs disrupts the cellular interactions and leads to skewed muscle niche with aggravated muscle dystrophy upon chronic injury.
2024-11-27 | GSE250203 | GEO
Project description:Adult skeletal muscle stem cells (MuSCs), also known as satellite cells (SCs), are widely believed to be responsible for muscle regeneration, which is regulated by complex networks of intrinsic and extrinsic factors. Emerging evidence demonstrates extrinsic regulations from other cell types can significantly impact the regeneration process, especially in repetitive cycles of degeneration/regeneration environment. Here, we demonstrate that the transcription factor (TF) Yin Yang 1 (YY1) deletion in MuSCs of mdx mouse induces CCL5 expression by alleviating the repressive effect on 3D structural interactions on Ccl5 locus. This leads to the increased secretion of CCL5 from MuSCs to the muscle niche, which promotes the recruitment of macrophages (MPs) through the CCL5/CCR5 axis. Incremental MPs lead to continuous inflammation that promotes the survival of Fibro-adipogenic progenitors’ (FAP) through secreting elevated TGFβ1 to stimulate FAPs resisting apoptosis, resulting in aggravated dystrophic pathology manifested by exacerbated fibrosis. Inhibition of CCL5/CCR5 axis by Maraviroc injection effectively mitigates muscle dystrophy and enhances muscle performance in YY1 deletion mdx mouse. Altogether, our findings promote us to conclude that YY1 functions as a 3D structural protein to repress Ccl5 production at the transcriptional level in MuSCs, playing a critical role in orchestrating MuSC/MP/FAP crosstalk through CCL5/CCR5 and TGFβ1 signaling. Intrinsic deletion of YY1 in MuSCs disrupts the cellular interactions and leads to skewed muscle niche with aggravated muscle dystrophy upon chronic injury.
2024-11-27 | GSE250202 | GEO
Project description:Adult skeletal muscle stem cells (MuSCs), also known as satellite cells (SCs), are widely believed to be responsible for muscle regeneration, which is regulated by complex networks of intrinsic and extrinsic factors. Emerging evidence demonstrates extrinsic regulations from other cell types can significantly impact the regeneration process, especially in repetitive cycles of degeneration/regeneration environment. Here, we demonstrate that the transcription factor (TF) Yin Yang 1 (YY1) deletion in MuSCs of mdx mouse induces CCL5 expression by alleviating the repressive effect on 3D structural interactions on Ccl5 locus. This leads to the increased secretion of CCL5 from MuSCs to the muscle niche, which promotes the recruitment of macrophages (MPs) through the CCL5/CCR5 axis. Incremental MPs lead to continuous inflammation that promotes the survival of Fibro-adipogenic progenitors’ (FAP) through secreting elevated TGFβ1 to stimulate FAPs resisting apoptosis, resulting in aggravated dystrophic pathology manifested by exacerbated fibrosis. Inhibition of CCL5/CCR5 axis by Maraviroc injection effectively mitigates muscle dystrophy and enhances muscle performance in YY1 deletion mdx mouse. Altogether, our findings promote us to conclude that YY1 functions as a 3D structural protein to repress Ccl5 production at the transcriptional level in MuSCs, playing a critical role in orchestrating MuSC/MP/FAP crosstalk through CCL5/CCR5 and TGFβ1 signaling. Intrinsic deletion of YY1 in MuSCs disrupts the cellular interactions and leads to skewed muscle niche with aggravated muscle dystrophy upon chronic injury.
2024-11-27 | GSE250197 | GEO
Project description:Adult skeletal muscle stem cells (MuSCs), also known as satellite cells (SCs), are widely believed to be responsible for muscle regeneration, which is regulated by complex networks of intrinsic and extrinsic factors. Emerging evidence demonstrates extrinsic regulations from other cell types can significantly impact the regeneration process, especially in repetitive cycles of degeneration/regeneration environment. Here, we demonstrate that the transcription factor (TF) Yin Yang 1 (YY1) deletion in MuSCs of mdx mouse induces CCL5 expression by alleviating the repressive effect on 3D structural interactions on Ccl5 locus. This leads to the increased secretion of CCL5 from MuSCs to the muscle niche, which promotes the recruitment of macrophages (MPs) through the CCL5/CCR5 axis. Incremental MPs lead to continuous inflammation that promotes the survival of Fibro-adipogenic progenitors’ (FAP) through secreting elevated TGFβ1 to stimulate FAPs resisting apoptosis, resulting in aggravated dystrophic pathology manifested by exacerbated fibrosis. Inhibition of CCL5/CCR5 axis by Maraviroc injection effectively mitigates muscle dystrophy and enhances muscle performance in YY1 deletion mdx mouse. Altogether, our findings promote us to conclude that YY1 functions as a 3D structural protein to repress Ccl5 production at the transcriptional level in MuSCs, playing a critical role in orchestrating MuSC/MP/FAP crosstalk through CCL5/CCR5 and TGFβ1 signaling. Intrinsic deletion of YY1 in MuSCs disrupts the cellular interactions and leads to skewed muscle niche with aggravated muscle dystrophy upon chronic injury.
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Project description:Mitochondrial biogenesis requires precise regulation of both mitochondrial-encoded and nuclear-encoded genes. Nuclear receptor Nur77 is known to regulate mitochondrial metabolism in macrophages and skeletal muscle cells. Here, we compared genome-wide Nur77 binding site and target gene expression in these two cell types, which revealed conserved roles for this nuclear receptor in the regulation of nuclear-encoded mitochondrial ribosomal proteins (MRP) and enrichment of motifs for the transcription factor Yin-Yang 1 (YY1). We show that Nur77 and YY1 interact, that YY1 increases Nur77 activity, and that their binding sites are co-enriched at MRP gene loci. Nur77 and YY1 co-expression synergistically increases mitochondrial abundance and activity in macrophages but not skeletal muscle. As such, we identify a macrophage-specific Nur77-YY1 interaction that enhances mitochondrial metabolism.
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