MiRNA expression profiles of PRC SiRNA vs scramble transfected XTC.UC1 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE33843 | GEO | 2011/11/22
SECONDARY ACCESSION(S): PRJNA148189
REPOSITORIES: GEO
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Project description:PGC-1 related coactivator (PRC) shares structural and functional features with PGC-1{alpha}. It regulates several metabolic pathways and mitochondrial biogenesis. Its specific role in the early programming of cell proliferation suggests a finely regulated crosstalk between the mitochondrial functions and the cell cycle status. To explore the PRC-regulated pathways, we used a cell-line model of mitochondrial-rich tumors, presenting an oxidative metabolism and a specific increase in PRC expression. We looked for the feedback loop exerted by miRNAs on the regulation of PRC-related mitochondiral functions Expression profiles of miRNA at 48h PRC SIRNA treatment compared to scramble in XTC.UC1 cells. In duplicate.
2011-11-22 | E-GEOD-33843 | biostudies-arrayexpress
Project description:PGC-1 related coactivator (PRC) shares structural and functional features with PGC-1{alpha}. It regulates several metabolic pathways and mitochondrial biogenesis. Its specific role in the early programming of cell proliferation suggests a finely regulated crosstalk between the mitochondrial functions and the cell cycle status. To explore the PRC-regulated pathways, we used a cell-line model of mitochondrial-rich tumors, presenting an oxidative metabolism and a specific increase in PRC expression. Microarray studies of temporal PRC invalidation in these XTC.UC1 cells were compared to the functional status of the mitochondria as well as to the expression level of genes and proteins involved in the oxidative phosphorylation process. Compared with what was observed for PGC-1{alpha}, we explored the role of nitric oxide in the PRC-regulated mitochondrial biogenesis. We proved that nitric oxide rapidly influences the expression of PRC at the transcriptional level. Focusing on mitochondrial energy metabolism, we demonstrated that PRC differentially controls the respiratory chain complexes and the coupling efficiency, in order to conserve a sufficient level of ATP and to protect the cell from oxidative stress. Our results highlight the key role of the PRC coactivator in the fine modulation of metabolic functions in response to the cell cycle status. Keywords: Transcriptionnal coactivator invalidation by SiRNA Expression profiles at 0h, 12h, 24h and 48h of PRC SIRNA treatment compared to scramble and referred to time of 20% serum induction. Expression profiles of PRC SIRNA and scramble during serum starvation were referred as -1.
2010-05-14 | E-GEOD-14282 | biostudies-arrayexpress
Project description:PGC-1 related coactivator (PRC) shares structural and functional features with PGC-1{alpha}. It regulates several metabolic pathways and mitochondrial biogenesis. Its specific role in the early programming of cell proliferation suggests a finely regulated crosstalk between the mitochondrial functions and the cell cycle status. To explore the PRC-regulated pathways, we used a cell-line model of mitochondrial-rich tumors, presenting an oxidative metabolism and a specific increase in PRC expression. Microarray studies of temporal PRC invalidation in these XTC.UC1 cells were compared to the functional status of the mitochondria as well as to the expression level of genes and proteins involved in the oxidative phosphorylation process. Compared with what was observed for PGC-1{alpha}, we explored the role of nitric oxide in the PRC-regulated mitochondrial biogenesis. We proved that nitric oxide rapidly influences the expression of PRC at the transcriptional level. Focusing on mitochondrial energy metabolism, we demonstrated that PRC differentially controls the respiratory chain complexes and the coupling efficiency, in order to conserve a sufficient level of ATP and to protect the cell from oxidative stress. Our results highlight the key role of the PRC coactivator in the fine modulation of metabolic functions in response to the cell cycle status. Keywords: Transcriptionnal coactivator invalidation by SiRNA
2009-01-07 | GSE14282 | GEO
Project description:Mammalian PGC-1alpha, PGC-1beta and PRC are structurally related transcriptional coactivators, and are involved in multiple metabolic functions, including the regulation of mitochondrial biogenesis. However, due to redundancy, their in vivo roles are still poorly understood. By a genome-wide microarray study, we show that in the Drosophila larval fat body, Spargel (CG9809), the only fly PGC-1 family homologue, is required for proper expression of multiple genes encoding mitochondrial proteins. Experiment Overall Design: Six samples were analyzed in total: three biological replicates of the control (wt) and three biological replicates of the mutant (KG).
2009-02-21 | E-GEOD-14780 | biostudies-arrayexpress
Project description:Mammalian PGC-1alpha, PGC-1beta and PRC are structurally related transcriptional coactivators, and are involved in multiple metabolic functions, including the regulation of mitochondrial biogenesis. However, due to redundancy, their in vivo roles are still poorly understood. By a genome-wide microarray study, we show that in the Drosophila larval fat body, Spargel (CG9809), the only fly PGC-1 family homologue, is required for proper expression of multiple genes encoding mitochondrial proteins.
2009-02-13 | GSE14780 | GEO
Project description:PRC, a member of the PGC-1 coactivator family, is responsive to serum growth factors and up regulated in proliferating cells. Here, we investigated its in vivo role by stably silencing PRC expression with two different short hairpin RNAs (shRNA#1 and shRNA#4) that were lentivirally introduced into U2OS cells. ShRNA#1 transductants exhibited nearly complete knockdown of PRC protein whereas shRNA#4 transductants expressed PRC protein at approximately 15 percent of the control level. Complete PRC silencing by shRNA#1 resulted in a severe inhibition of respiratory growth, reduced expression of respiratory protein subunits from complexes I, II, III and IV, markedly lower complex I and IV respiratory enzyme levels and diminished mitochondrial ATP production. Surprisingly, shRNA#1 transductants exhibited a striking proliferation of abnormal mitochondria that were devoid of organized cristae and displayed severe membrane abnormalities. Although shRNA#4 transductants had normal respiratory subunit expression and a moderately diminished respiratory growth rate, both transductants showed markedly reduced growth on glucose accompanied by inhibition of G1/S cell cycle progression. Microarray analysis revealed striking overlaps in the genes affected by PRC silencing in the two transductants and the functional identities of these overlapping genes were consistent with the observed mitochondrial and cell growth phenotypes. The consistency between phenotype and PRC expression levels in the two independent transductant lines argues that the defects result from PRC silencing and not from off target effects. These results support a role for PRC in the integration of pathways directing mitochondrial respiratory function and cell growth.
2009-01-16 | GSE14428 | GEO
Project description:Decreased mitochondrial mass and function in muscle of diabetic patients is associated with low PGC-1alpha, a transcriptional coactivator of the mitochondrial gene program. To investigate whether reduced PGC-1alpha and oxidative capacity in muscle directly contributes to age-related glucose intolerance, we compared the genetic signatures and metabolic profiles of aging mice lacking muscle PGC-1alpha. Microarray analysis revealed that a significant proportion of PGC-1alpha-dependent changes in gene expression overlapped with age-associated effects, and aging muscle and muscle lacking PGC-1alpha shared gene signatures of impaired electron transport chain activity and TGFbeta signalling. Gastrocnemius muscle mRNA from young (10 week old) and old (24 month old) wild-type and knock-out (muscle-specific PGC-1alpha, myogenin-cre) C57Bl/6N/6J/129 mice
2013-12-05 | E-GEOD-52550 | biostudies-arrayexpress
Project description:The following abstract from the submitted manuscript describes the major findings of this work. The metabolic development of high energy-utilizing organs such as the heart involves mitochondrial proliferation at birth followed by a maturation process during the postnatal period. Conditional gene targeting was used in mice to explore the role of the PPARgamma coactivator 1 (PGC-1) coactivators during postnatal development and in adult heart. Marked mitochondrial derangements were observed in hearts of PGC-1a/b-deficient mice during the postnatal period, including fragmentation and elongation associated with the development of a lethal cardiomyopathy. The expression of multiple genes involved in mitochondrial fusion and fission was downregulated in hearts of PGC-1a/b-deficient mice. PGC-la was shown to activate transcription of the mitofusin 1 (Mfn1) gene by coactivating the estrogen-related receptor a (ERRa) upon a highly conserved element. Surprisingly, PGC-1a/b deficiency did not alter cardiac function or general mitochondrial density and myocyte distribution in adult heart. However, transcriptional profiling and mitochondrial function studies demonstrated that the PGC-1 coactivators are required for full respiratory capacity and high level expression of nuclear- and mitochondrial-encoded genes involved in mitochondrial energy transduction and oxidative phosphorylation pathways in adult heart. These results unveil distinct developmental stage-specific transcriptional programs involved in the maturation and maintenance of mitochondria. RNA from five PGC-1a-/- and five PGC-1a-/-bf/f/MerCre mice was analyzed.
2014-01-13 | E-GEOD-43798 | biostudies-arrayexpress
Project description:Amyotrophic later sclerosis is a motor neuron disease accompanied by metabolic changes. PGC (PPAR gamma coactivator)-1alpha is a master regulator of mitochondrial biogenesis and function and of critical importance for all metabolically active tissues. PGC-1alpha is a genetic modifier of ALS. We used microarray analysis to identify PGC-1alpha target genes in the brain.
2016-11-10 | GSE77919 | GEO
Project description:Decreased mitochondrial mass and function in muscle of diabetic patients is associated with low PGC-1alpha, a transcriptional coactivator of the mitochondrial gene program. To investigate whether reduced PGC-1alpha and oxidative capacity in muscle directly contributes to age-related glucose intolerance, we compared the genetic signatures and metabolic profiles of aging mice lacking muscle PGC-1alpha. Microarray analysis revealed that a significant proportion of PGC-1alpha-dependent changes in gene expression overlapped with age-associated effects, and aging muscle and muscle lacking PGC-1alpha shared gene signatures of impaired electron transport chain activity and TGFbeta signalling.
2013-12-05 | GSE52550 | GEO