The transcriptional coregulator PGC-1β controls mitochondrial function and anti-oxidant defense in skeletal muscles
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE73572 | GEO | 2015/12/16
SECONDARY ACCESSION(S): PRJNA297347
REPOSITORIES: GEO
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Project description:Transcriptional microarray analysis was conducted on gastrocnemius muscle of control and PGC-1β(i)skm-/- mice one week after the last tamoxifen administration using the Affymetrix Mouse Gene 1.0 ST. each sample represent a pool of 3 different mice.
2015-12-16 | E-GEOD-73572 | biostudies-arrayexpress
Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in enterocytes from intestine specific PGC-1β konckout mice. Total RNA obtained from ileum samples from IKOPGC-1β mice was compared to the total RNA extracted from their wild-type littermates.
2015-03-01 | E-GEOD-61640 | biostudies-arrayexpress
Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in enterocytes from intestine specific PGC-1β konckout mice.
2015-03-01 | GSE61640 | GEO
Project description:The transcriptional coregulators PGC-1? and PGC-1? modulate the expression of numerous partially overlapping genes involved in mitochondrial biogenesis and energetic metabolism. The physiological role of PGC-1? is poorly understood in skeletal muscle, a tissue of high mitochondrial content to produce ATP levels required for sustained contractions. Here we determine the physiological role of PGC-1? in skeletal muscle using mice, in which PGC-1? is selectively ablated in skeletal myofibres at adulthood (PGC-1?((i)skm-/-) mice). We show that myofibre myosin heavy chain composition and mitochondrial number, muscle strength and glucose homeostasis are unaffected in PGC-1?((i)skm-/-) mice. However, decreased expression of genes controlling mitochondrial protein import, translational machinery and energy metabolism in PGC-1?((i)skm-/-) muscles leads to mitochondrial structural and functional abnormalities, impaired muscle oxidative capacity and reduced exercise performance. Moreover, enhanced free-radical leak and reduced expression of the mitochondrial anti-oxidant enzyme Sod2 increase muscle oxidative stress. PGC-1? is therefore instrumental for skeletal muscles to cope with high energetic demands.
| S-EPMC4703903 | biostudies-literature
Project description:Hepatic microRNA Expression by PGC-1α and PGC-1β in the Mouse II
| PRJNA595599 | ENA
Project description:Hepatic microRNA Expression by PGC-1α and PGC-1β in the Mouse I
| PRJNA595600 | ENA
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:Peroxisome proliferator-activated receptor-gamma coactivator-1β (PGC-1β) is a transcriptional regulator whose increased expression activates energy expenditure-related genes in skeletal muscles. However, how PGC-1β is regulated remains largely unclear. Here, we show that PGC-1β gene expression is negatively correlated with the expression of a transcription factor, forkhead box protein O1 (FOXO1), whose expression is increased during muscle atrophy. In the skeletal muscles of FOXO1-overexpressing transgenic mice, PGC-1β gene expression is decreased. Denervation or plaster cast-based unloading, as well as fasting, increases endogenous FOXO1 expression in skeletal muscles, with decreased PGC-1β expression. In the skeletal muscles of FOXO1-knockout mice, the decrease in PGC-1β expression caused by fasting was attenuated. Tamoxifen-inducible FOXO1 activation in C2C12 myoblasts causes a marked decrease of PGC-1β expression. These findings together reveal that FOXO1 activation suppresses PGC-1β expression. During atrophy with FOXO1 activation, decreased PGC-1β may decrease energy expenditure and avoid wasting energy.
| S-EPMC7327905 | biostudies-literature
Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in enterocytes from transgenic mice overexpressing PGC-1β specifically in the intestine. Total RNA obtained from ileum samples from iPGC-1β mice was compared to the total RNA extracted from their wild-type littermates.
2015-03-01 | E-GEOD-61641 | biostudies-arrayexpress
Project description:Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1α. We could then efficiently knockdown PGC-1β expression by shRNA expression. Loss of PGC-1α did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. Cells deficient in either PGC-1α or PGC-1β coactivators showed a small decrease in the differentiation-dependant program of mitochondrial biogenesis and respiration; however, this increase in mitochondrial number and function was totally abolished during brown fat differentiation when both PGC-1α and PGC-1β were deficient. These data show that PGC-1α is essential for brown fat thermogenesis but not brown fat differentiation, and the PGC-1 coactivators play an absolutely essential but complementary function in differentiation-induced mitochondrial biogenesis. Affymetrix microarray analysis of total RNA from wt, PGC-1α KO and PGC-1α KO cells expressing an RNAi specific for PGC-1β knockdown was performed. Of the 461 mitochondrial genes analyzed, 181 were found to be at least 20% different between wt and defective PGC-1α and β adipocytes (p < 0.05). More than 85% of these genes were downregulated in cells deficient for PGC-1alpha and PGC-1beta. Keywords: Analysis of mitochondrial gene expression
2006-07-06 | GSE5042 | GEO