Mus musculus
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PROVIDER: PRJNA288810 | ENA |
REPOSITORIES: ENA
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Project description:Title: Total Skeletal Muscle PGC-1 Deficiency Uncouples Mitochondrial Derangements from Fiber Type Determination and Insulin Sensitivity Abstract: Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1α-/- βf/f/MLC-Cre mice) were generated and characterized. PGC-1α-/-βf/f/MLC-Cre mice exhibit a dramatic reduction in exercise performance compared to single PGC-1α- or PGC-1β-deficient mice and wild-type controls. The exercise phenotype of the PGC-1α-/-βf/f/MLC-Cre mice was associated with a marked diminution in muscle oxidative capacity and mitochondrial structural derangements consistent with fusion/fission and biogenic defects together with rapid depletion of muscle glycogen stores during exercise. Surprisingly, the skeletal muscle fiber type profile of the PGC-1α-/-βf/f/MLCCre mice was not significantly different than the wild-type mice. Moreover, insulin sensitivity and glucose tolerance were also not altered in the PGC-1α-/-βf/f/MLC-Cre mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity.
2010-12-01 | GSE23365 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description:Title: Total Skeletal Muscle PGC-1 Deficiency Uncouples Mitochondrial Derangements from Fiber Type Determination and Insulin Sensitivity Abstract: Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1α-/- βf/f/MLC-Cre mice) were generated and characterized. PGC-1α-/-βf/f/MLC-Cre mice exhibit a dramatic reduction in exercise performance compared to single PGC-1α- or PGC-1β-deficient mice and wild-type controls. The exercise phenotype of the PGC-1α-/-βf/f/MLC-Cre mice was associated with a marked diminution in muscle oxidative capacity and mitochondrial structural derangements consistent with fusion/fission and biogenic defects together with rapid depletion of muscle glycogen stores during exercise. Surprisingly, the skeletal muscle fiber type profile of the PGC-1α-/-βf/f/MLCCre mice was not significantly different than the wild-type mice. Moreover, insulin sensitivity and glucose tolerance were also not altered in the PGC-1α-/-βf/f/MLC-Cre mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity. RNA from PGC-1alpha-/- beta f/f/Mlc1fcre was obtained and gene expression pattern compared with PGC-1alpha -/-, PGC-1beta f/f, and PGC-1beta f/f/Mlc1fCre controls. Results file descriptions: 1. GSE23365_skfloxAKO_PPexcl_genesup_GEO-8-16-2010: This table contains genes that were upregulated ≥2.0 fold in gastrocnemius muscle from PGC-1alpha-/- - mice, PGC-1beta f/f/Mlc1fCre mice and PGC-1alpha-/- - beta f/f/Mlc1fCre mice. All groups are normalized to PGC-1beta f/f mice and values are expressed as mean±SEM. The column “description’ contains the gene name, and the column “ID” contains Agilent probe names. 2. GSE23365_skfloxAKO_PPexcl_genesdown_GEO-8-16-2010 This table contains genes that were downregulated ≤0.7 fold in gastrocnemius muscle from PGC-1alpha-/- - mice, PGC-1beta f/f/Mlc1fCre mice and PGC-1alpha-/- - beta f/f/Mlc1fCre mice. All groups are normalized to PGC-1beta f/f mice and values are expressed as mean±SEM. The column “description’ contains the gene name, and the column “ID” contains Agilent probe names.
2010-12-01 | E-GEOD-23365 | biostudies-arrayexpress
Project description:This experiment was conducted to identify novel MLL4 targets in skeletal muscle Enhancers play central role in controlling gene expression in time and space. Primed enhancers are marked by histone H3 lysine 4 (H3K4) mono/di-methylation (H3K4me1/2). Mixed-lineage leukemia 4 (MLL4/KMT2D) is an evolutionarily conserved H3K4me1/2 methyltransferase that is required for enhancer activation. Here, we identified the genome-wide MLL4 occupancy in mouse skeletal muscle by ChIP-seq coupled with RNA-seq analysis. Gene ontology analysis revealed that MLL4 controls muscle fiber-type switching. We thus have revealed novel MLL4 targets involved in muscle metabolism.
2020-10-01 | GSE138994 | GEO
Project description:This experiment was conducted to identify target microRNAs of the peroxisome proliferator-activated receptor (PPAR) in skeletal muscle of transgenic mice that overexpressed PPARalpha or PPARbeta. We have recently demonstrated that skeletal muscle-specific PPARb transgenic (MCK-PPARb) mice exhibit increased exercise endurance, whereas MCK-PPARa mice have reduced exercise performance. Accordingly, we sought to determine whether PPARb and PPARa drive distinct programs involved in muscle fiber type determination. Myosin heavy chain (MHC) immunohistochemical staining of soleus muscle revealed a marked increase in type 1 fibers in the MCK-PPARb muscle compared to non-transgenic (NTG) littermates but a profound reduction in MCK-PPARa muscle. miRNA profiling revealed that levels of miR-208b and miR-499 were increased in MCK-PPARb muscle but reduced in MCK-PPARa muscle. miR-208b and miR-499, which are embedded in the Myh7 and Myh7b genes, respectively, have been shown previously to regulate slow-twitch muscle genes. Lastly, combined inhibition of miR-208b and miR-499 abolished the enhancing effects of PPARb on MHC1 expression in skeletal myotubes, while forced expression of miR-499 in MCK-PPARa muscle completely reversed the type 1 fiber program and exercise capacity. Taken together, these findings demonstrate that miR-208b and miR-499 are necessary to mediate the effects of PPARb and PPARa on muscle fiber type determination.
2013-05-09 | GSE36498 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2024-11-07 | MSV000096332 | MassIVE
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2024-11-07 | MSV000096331 | MassIVE
Project description:This experiment was conducted to identify target microRNAs of the peroxisome proliferator-activated receptor (PPAR) in skeletal muscle of transgenic mice that overexpressed PPARalpha or PPARbeta. We have recently demonstrated that skeletal muscle-specific PPARb transgenic (MCK-PPARb) mice exhibit increased exercise endurance, whereas MCK-PPARa mice have reduced exercise performance. Accordingly, we sought to determine whether PPARb and PPARa drive distinct programs involved in muscle fiber type determination. Myosin heavy chain (MHC) immunohistochemical staining of soleus muscle revealed a marked increase in type 1 fibers in the MCK-PPARb muscle compared to non-transgenic (NTG) littermates but a profound reduction in MCK-PPARa muscle. miRNA profiling revealed that levels of miR-208b and miR-499 were increased in MCK-PPARb muscle but reduced in MCK-PPARa muscle. miR-208b and miR-499, which are embedded in the Myh7 and Myh7b genes, respectively, have been shown previously to regulate slow-twitch muscle genes. Lastly, combined inhibition of miR-208b and miR-499 abolished the enhancing effects of PPARb on MHC1 expression in skeletal myotubes, while forced expression of miR-499 in MCK-PPARa muscle completely reversed the type 1 fiber program and exercise capacity. Taken together, these findings demonstrate that miR-208b and miR-499 are necessary to mediate the effects of PPARb and PPARa on muscle fiber type determination. Comparison of microRNA expression from soleus muscles isolated from wild-type (non-transgenic (NTG)) and PPARalpha-overexpressing (MCK-PPARa) mice, and comparison of microRNA expression from soleus muscles isolated from wild-type (NTG) and PPARbeta-overexpressing (MCK-PPARb) mice. Three replicates of each are analyzed.
2013-05-09 | E-GEOD-36498 | biostudies-arrayexpress
Project description:Aberrant calcium influx causes fiber type shift and mitochondrial loss in skeletal muscle
| PRJNA280959 | ENA