Evidence map›Paper›PMID 19956726›Full record

ArticlePloS one2009

PGC-1-related coactivator modulates mitochondrial-nuclear crosstalk through endogenous nitric oxide in a cellular model of oncocytic thyroid tumours.

Mahatsangy Raharijaona, Soazig Le Pennec, Julie Poirier, Delphine Mirebeau-Prunier, Clothilde Rouxel, Caroline Jacques, Jean-Fred Fontaine, Yves Malthiery, Rémi Houlgatte, Frédérique Savagner

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. TheBiomolecules · 2025
    Review
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  8. NO control of mitochondrial function in normal and transformed cells.Biochimica et biophysica acta. Bioenergetics · 2017
    Review
  9. Review
  10. miR-199a-5p regulatesOncology letters · 2016
    Article
  11. Article
  12. Article
  13. Transcriptional integration of mitochondrial biogenesis.Trends in endocrinology and metabolism: TEM · 2012
    Review
  14. Article
  15. Review
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Mahatsangy RaharijaonaINSERM, UMR 915, l'Institut du Thorax, Nantes, France.
Soazig Le Pennec
Julie Poirier
Delphine Mirebeau-Prunier
Clothilde Rouxel
Caroline Jacques
Jean-Fred Fontaine
Yves Malthiery
Rémi Houlgatte
Frédérique Savagner
Inserm · FRUniversité d'Angers · FRInstitut du Thorax · FRNantes Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe PGC-1 related coactivator (PRC), which shares structural and functional features with PGC-1alpha, is believed to regulate several metabolic pathways as well as mitochondrial biogenesis. Its involvement in the early programming of cell proliferation suggests the existence of finely regulated crosstalk between mitochondrial functions and the cell cycle status. METHODOLOGY/PRINCIPAL

findingsPRC-regulated pathways were explored in a cell-line model derived from mitochondrial-rich tumours with an essentially oxidative metabolism and specifically high PRC expression. The functional status of mitochondria was compared to the results of microarray analysis under conditions of temporal PRC inhibition. To specify the fine PRC regulation, the expression levels of the genes and proteins involved in the oxidative phosphorylation process were studied by real time quantitative PCR and western blotting. As in earlier studies on PGC-1alpha, we investigated the role of nitric oxide in PRC-regulated mitochondrial biogenesis and determined its action in the control of the phosphorylation status of the mitogen-activated protein kinase pathway. CONCLUSION/SIGNIFICANCE: We found that nitric oxide rapidly influences PRC expression at the transcriptional level. Focusing on mitochondrial energetic metabolism, we observed that PRC differentially controls respiratory chain complexes and coupling efficiency in a time-dependent manner to maintain mitochondrial homeostasis. Our results highlight the key role of PRC in the rapid modulation of metabolic functions in response to the status of the cell cycle.

Indexed as

Cell CycleCell Cycle ProteinsCell NucleusCluster AnalysisElectron TransportFlow CytometryGene Expression RegulationHumansMAP Kinase Signaling SystemMitochondriaNitric OxideOligonucleotide Array Sequence AnalysisPhosphorylationReverse Transcriptase Polymerase Chain ReactionThyroid NeoplasmsCell Cycle ProteinsNitric OxidePRC1 protein, human

Identifiers

PMID19956726
PMCPMC2776512
OpenAlexW2018948517

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.