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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE65993 | GEO | 2015/02/18

SECONDARY ACCESSION(S): PRJNA275649

REPOSITORIES: GEO

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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

Mus musculus

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

| PRJNA275649 | ENA

Expression data from Arabidopsis thaliana treated with NO donor SNP, compared to NO depletion by cPTIO

Project description:Nitric oxide (NO) is considered a key regulator of plant developmental processes and defense. Characterization of root-related phenotypes and the involvement of NO in the regulation of primary root growth. Three-experimental condition, SDW, SNP and cPTIO. Biological replicates: 3 control replicates (SDW) , 3 replicates treated with sodium nitroprusside (SNP), 3 replicates treated with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO)

2015-12-21 | E-GEOD-21556 | biostudies-arrayexpress

Nitric oxide-dependent changes in Schistosoma mansoni gene expression

2007-07-04 | GSE8366 | GEO

Transcriptome response to nitrosative stress in Rhodobacter sphaeroides 2.4.1

Project description:DNA microarray analysis was employed to investigate the transcriptome response to nitrosative stress in a non-denitrifying facultative photosynthetic bacterium Rhodobacter sphaeroides 2.4.1. We focused on the role played by a nitric oxide-response transcriptional regulator NnrR in the response. The transcriptome profiles of R. sphaeroides 2.4.1 and its nnrR mutant before and after exposure to nitrosating agents S-nitrosoglutathione (GSNO) or sodium nitroprusside (SNP) under semiaerobic conditions were analyzed.

2012-11-11 | GSE33641 | GEO

Nitric oxide-dependent changes in Schistosoma mansoni gene expression

Project description:Nitric oxide (NO) is a gaseous intercellular signaling molecule that also plays a role in host-parasite relations. NO acts rapidly, either via regulation of soluble guanylate cyclase, or by direct interactions with enzymes and other proteins, and has also been shown to have effects on gene expression. Here, we use SAGE (Serial Analysis of Gene Expression) to identify NO-responsive changes in gene expression in Schistosoma mansoni following a 3 hour exposure to sodium nitroprusside, an NO donor. Overall, these results indicate that NO does not rapidly induce large-scale changes in schistosome gene expression, but that expression of particular genes of interest appear to respond to NO. Keywords: Schistosoma, SAGE, NOS, nitric oxide, gene expression Adult S. mansoni perfused from infected Swiss-Webster female mice (obtained from the NIAID Schistosomiasis Resource Center) 42-49 days postinfection were maintained in culture (RPMI medium) overnight and then exposed for 3 hours to either 1 mM sodium nitroprusside (SNP), a well-characterized NO donor, or to RPMI alone. Worms remained viable and motile following treatment. Total RNA was extracted with Trizol (Invitrogen) and treated with DNAse 1 (Ambion) to remove contaminating genomic DNA, and Long-SAGE libraries constructed.

2007-07-04 | E-GEOD-8366 | biostudies-arrayexpress

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

PRC SiRNA vs scramble transfection in XTC.UC1 cells

2009-01-07 | GSE14282 | GEO

Skeletal muscle PGC-1a mediates mitochondrial, but not metabolic, changes during calorie restriction.

Project description:Calorie restriction (CR) is a dietary intervention that extends lifespan and healthspan in a variety of organisms. CR improves mitochondrial energy production, fuel oxidation and reactive oxygen species scavenging in skeletal muscle and other tissues, and these processes are thought to be critical to the benefits of CR. PGC-1a is a transcriptional coactivator that regulates mitochondrial function and is induced by CR. Consequently, many of the mitochondrial and metabolic benefits of CR are attributed to increased PGC-1a activity. To test this model for the first time, we examined the metabolic and mitochondrial response to CR in mice lacking skeletal muscle PGC-1a (MKO). Surprisingly, MKO mice demonstrated a normal improvement in glucose homeostasis in response to CR, indicating that skeletal muscle PGC-1a is dispensable for the whole-body benefits of CR. In contrast, gene expression profiling and electron microscopy demonstrated that PGC-1a is required for the full CR-induced increases in mitochondrial gene expression and mitochondrial density in skeletal muscle. These results demonstrate that PGC-1a is a major regulator of the mitochondrial response to CR in skeletal muscle, but surprisingly show that neither PGC-1a nor mitochondrial biogenesis in skeletal muscle are required for the metabolic benefits of CR. Control (FLOX) and PGC-1a skeletal muscle specific knock out (MKO) mice were placed on a control diet [C] or a calorie restriction diet [CR] for 12 weeks. RNA was isolated from TA/EDL muscles for microarray analysis. The following numbers of mice were analyzed from each group: C FLOX: n = 6; C MKO: n = 7; CR FLOX: n = 6; CR MKO: n = 7. Mice were mixed C57/BL6 and 129 background.

2012-02-04 | E-GEOD-34773 | biostudies-arrayexpress

Transcription profiling of pig coronary arterial endothelial cells by multiple passaging in vitro

Project description:Nitric oxide helps to prevent endothelial dysfunction and senescence. This study aimed to define genomic and proteomic changes in cultured porcine senescent endothelial cells and their resemblance with those observed in regenerated endothelial cells. Senescent endothelial cells were produced by passaging primary porcine coronary arterial endothelial cells until passage four. The protein presence of endothelial nitric oxide synthase, cyclic GMP levels [basal and during stimulation (bradykinin and A23187)], were reduced. The mRNA expression level was measured by microarray assays. Genes related to oxidative stress [superoxide dismutase (MnSOD), glutathione peroxidase 3, glutathione S-transferase M1] were downregulated, extracellular matrix components (type III collagen, thrombospondin 1 and 3, transforming growth factor ?) upregulated and nuclear factor kappa B (NF?B)-signaling pathway [IkappaB, TNF receptor-associated factor 1 and 5 (TRAF1 and 5)] activated in senescent cells. The differential gene expression of MnSOD and TRAF5 was confirmed at the protein level by Western blotting and biochemical assay (MnSOD). The basal and stimulated (by tumor necrosis factor-?)?levels of NF?B were augmented as demonstrated by electrophoretic mobility shift assay. In summary, cultured senescent endothelial cells exhibit reduced nitric oxide production, and decreased antioxidative, proliferative capacities, augmented expression of extracellular matrix components and activation of NF?B. These molecular changes do not exactly mimick those occurring during endothelial regeneration in vivo. Experiment Overall Design: Totally 8 samples were analyzed with 4 replicates each for control (cells at passage one) and test (cells at passage four) samples.

2008-06-16 | E-GEOD-8974 | biostudies-arrayexpress

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