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PRC SiRNA vs scramble transfection in XTC.UC1 cells

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE14282 | GEO | 2009/01/07

SECONDARY ACCESSION(S): PRJNA111251

REPOSITORIES: GEO

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PRC SiRNA vs scramble transfection in XTC.UC1 cells

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

miRNA expression profiles of PRC SiRNA vs scramble transfected XTC.UC1 cells

2011-11-22 | E-GEOD-33843 | biostudies-arrayexpress

miRNA expression profiles of PRC SiRNA vs scramble transfected XTC.UC1 cells

2011-11-22 | GSE33843 | GEO

Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice

Project description:Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis. We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and to elicit the global antioxidative responses in mice. The large quantities of antioxidant enzymes are correlated with the low levels of reactive oxygen species, which allow the down-regulation of tumor suppressors and accessory DNA repair partners, eventually leading to the compromise of telomere shortening. Accompanying with the up-regulation of kinases, acetylases, and biomarkers, mitochondrial biogenesis occurs with the elevation of adenosine triphosphate levels upon exposure of mouse skeletal muscles to the mimetics of calorie restriction. In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity. Six samples were analyzed, in which a control sample was included.

2015-02-18 | E-GEOD-65993 | biostudies-arrayexpress

Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice

2015-02-18 | GSE65993 | GEO

Transcription profiling of Drosophila Spargel mutant versus genetically matched wildtype control

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

Gene expression analysis of spargel mutant versus genetically matched wildtype control

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Pyruvate induces mitochondrial biogenesis by a PGC-1alpha independent mechanism

Project description:The present study examines the impact of altering energy provision on mitochondrial biogenesis in muscle cells. C2C12 myoblasts were chronically treated with supraphysiological levels of sodium pyruvate for 72 hr. Treated cells exhibited increased mitochondrial protein expression, basal respiratory rate and maximal oxidative capacity. The increase in mitochondrial biogenesis was independent of increases in PGC-1alpha and PGC-1alpha mRNA expression. To further assess whether PGC-1alpha expression was necessary for pyruvate action, cells were infected with adenovirus containing shRNA for PGC-1alpha prior to treatment with pyruvate. Despite a 70% reduction in PGC-1alpha mRNA the effect of pyruvate was preserved. Furthermore, pyruvate induced mitochondrial biogenesis in primary myoblasts from PGC-1alpha null mice. These data suggest that regulation of mitochondrial biogenesis by pyruvate in myoblasts is independent of PGC-1alpha, suggesting the existence of a novel energy-sensing pathway regulating oxidative capacity. Keywords: basal state versus treatment at one time point

2006-08-12 | GSE5497 | GEO

Loss of renal tubular PGC-1α exacerbates diet-induced renal steatosis and age-related urinary sodium excretion in mice

Project description:The kidney has a high energy demand and is dependent on oxidative metabolism for ATP production. Accordingly, the kidney is rich in mitochondria, and mitochondrial dysfunction is a common denominator for several renal diseases. While the mitochondrial master regulator peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is highly expressed in kidney, its role in renal physiology is so far unclear. Here we show that PGC-1α is a central transcriptional regulator of mitochondrial metabolic pathways in the kidney. Moreover we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1α in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Overall, PGC-1α seems largely dispensable for basal renal physiology. However, the central role of PGC-1α in renal mitochondrial biogenesis indicates that activation of PGC-1α in the context of renal disorders could be a valid therapeutic strategy to ameliorate renal mitochondrial dysfunction.

2016-04-26 | GSE80618 | GEO

Remodeling of Brown and White Adipose Tissue by NT-PGC-1α-Mediated Gene Regulation

Project description:The β-adrenergic receptor signaling pathway is a major component of adaptive thermogenesis in brown and white adipose tissue during cold acclimation. The β-AR activation highly induces transcriptional coactivator PGC-1α and its splice variant N-terminal (NT)-PGC-1α, promoting the transcription program of mitochondrial biogenesis and thermogenesis. In the present study, we evaluated the role of NT-PGC-1α in brown adipocyte energy metabolism by genome-wide profiling of NT-PGC-1α-responsive genes. Canonical pathway analysis revealed that a number of genes upregulated by NT-PGC-1α are highly enriched in mitochondrial pathways including fatty acid transport and β-oxidation, TCA cycle and electron transport system, thus reinforcing the crucial role of NT-PGC-1α in the enhancement of mitochondrial function. Moreover, gene expression profiling of NT-PGC-1α revealed activation of distinct metabolic pathways such as glucose, lipid and nucleotide metabolism and of signaling pathways such as RAR and PPAR-γ/RXRα activation in brown adipocytes. Together, our data strengthen our previous findings that NT-PGC-1α is a key regulator of mitochondrial oxidative metabolism and thermogenesis in brown adipocytes and further suggest that NT-PGC-1α influences a broader spectrum of thermogenic processes to meet cellular needs for adaptive thermogenesis. Two samples from two groups: NT-PGC-1α overexpression and empty vector. There are technical replicates (A and B) for each group. Two RNA samples were pooled for each group.

2015-08-07 | E-GEOD-71774 | biostudies-arrayexpress

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