Evidence map›Paper›PMID 20849372›Full record

ArticleAntioxidants & redox signaling2011

Neuronal activity controls the antagonistic balance between peroxisome proliferator-activated receptor-γ coactivator-1α and silencing mediator of retinoic acid and thyroid hormone receptors in regulating antioxidant defenses.

Francesc X Soriano, Frédéric Léveillé, Sofia Papadia, Karen F S Bell, Clare Puddifoot, Giles E Hardingham

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Neuronal Activity and Its Role in Controlling Antioxidant Genes.International journal of molecular sciences · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. PGC-1α negatively regulates extrasynaptic NMDAR activity and excitotoxicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  12. Article
  13. Article
  14. Review
  15. The influence of synaptic activity on neuronal health.Current opinion in neurobiology · 2011
    Review
  16. Article
  17. Review
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

6 authors at 1 institution in 1 country.

Francesc X SorianoCentre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
Frédéric Léveillé
Sofia Papadia
Karen F S Bell
Clare Puddifoot
Giles E Hardingham
University of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research Council BB/D011388/1Medical Research Council G0902044Wellcome Trust 087491
6 · The paper itself

Abstract

Transcriptional coactivators and corepressors often have multiple targets and can have opposing actions on transcription and downstream physiological events. The coactivator peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is under-expressed in Huntington's disease and is a regulator of antioxidant defenses and mitochondrial biogenesis. We show that in primary cortical neurons, expression of PGC-1α strongly promotes resistance to excitotoxic and oxidative stress in a cell autonomous manner, whereas knockdown increases sensitivity. In contrast, the transcriptional corepressor silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) specifically antagonizes PGC-1α-mediated antioxidant effects. The antagonistic balance between PGC-1α and SMRT is upset in favor of PGC-1α by synaptic activity. Synaptic activity triggers nuclear export of SMRT reliant on multiple regions of the protein. Concomitantly, synaptic activity post-translationally enhances the transactivating potential of PGC-1α in a p38-dependent manner, as well as upregulating cyclic-AMP response element binding protein-dependent PGC-1α transcription. Activity-dependent targeting of PGC-1α results in enhanced gene expression mediated by the thyroid hormone receptor, a prototypical transcription factor coactivated by PGC-1α and repressed by SMRT. As a consequence of these events, SMRT is unable to antagonize PGC-1α-mediated resistance to oxidative stress in synaptically active neurons. Thus, PGC-1α and SMRT are antagonistic regulators of neuronal vulnerability to oxidative stress. Further, this coactivator-corepressor antagonism is regulated by the activity status of the cell, with implications for neuronal viability.

Indexed as

AnimalsAntioxidantsNeuronsNuclear Receptor Co-Repressor 2Oxidative Stressp38 Mitogen-Activated Protein KinasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionRNA-Binding ProteinsTranscription FactorsAntioxidantsNuclear Receptor Co-Repressor 2p38 Mitogen-Activated Protein KinasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratRNA-Binding Proteinssilencing mediator of retinoic acid and thyroid hormone receptors, ratTranscription Factors

Identifiers

PMID20849372
PMCPMC3044457
OpenAlexW2057879006

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.