Evidence map›Paper›PMID 24748101›Full record

ArticlePloS one2014

Histone acetylation and CREB binding protein are required for neuronal resistance against ischemic injury.

Ferah Yildirim, Shengbo Ji, Golo Kronenberg, Angel Barco, Roman Olivares, Eva Benito, Ulrich Dirnagl, Karen Gertz, Matthias Endres, Christoph Harms and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. CREB1ACS omega · 2021
    Article
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  8. Article
  9. Article
  10. Review
  11. Article
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  17. Oral administration of a novel lipophilic PPARδ agonist is not neuroprotective after rodent cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
  18. Article
  19. Review
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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

11 authors at 3 institutions in 2 countries.

Ferah YildirimDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Shengbo JiDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Golo KronenbergDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany; Klinik und Poliklinik für Psychiatrie, Campus Mitte, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Angel BarcoInstituto de Neurociencias de Alicante (Universidad Miguel Hernandez-Consejo Superior de Investigaciones Cientificas), Campus de Sant Joan, Sant Joan d'Alacant, Alicante, Spain.
Roman OlivaresInstituto de Neurociencias de Alicante (Universidad Miguel Hernandez-Consejo Superior de Investigaciones Cientificas), Campus de Sant Joan, Sant Joan d'Alacant, Alicante, Spain.
Eva BenitoInstituto de Neurociencias de Alicante (Universidad Miguel Hernandez-Consejo Superior de Investigaciones Cientificas), Campus de Sant Joan, Sant Joan d'Alacant, Alicante, Spain.
Ulrich DirnaglDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany; ExcellenceCluster NeuroCure, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Karen GertzDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany; ExcellenceCluster NeuroCure, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Matthias EndresDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany; ExcellenceCluster NeuroCure, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Christoph HarmsDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Andreas MeiselDepartment of Experimental Neurology, Center for Stroke Research Berlin (CSB) and Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Berlin, Germany; ExcellenceCluster NeuroCure, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEConsejo Superior de Investigaciones Científicas · ESInstituto de Neurociencias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic transcriptional regulation by histone acetylation depends on the balance between histone acetyltransferase (HAT) and deacetylase activities (HDAC). Inhibition of HDAC activity provides neuroprotection, indicating that the outcome of cerebral ischemia depends crucially on the acetylation status of histones. In the present study, we characterized the changes in histone acetylation levels in ischemia models of focal cerebral ischemia and identified cAMP-response element binding protein (CREB)-binding protein (CBP) as a crucial factor in the susceptibility of neurons to ischemic stress. Both neuron-specific RNA interference and neurons derived from CBP heterozygous knockout mice showed increased damage after oxygen-glucose deprivation (OGD) in vitro. Furthermore, we demonstrated that ischemic preconditioning by a short (5 min) subthreshold occlusion of the middle cerebral artery (MCA), followed 24 h afterwards by a 30 min occlusion of the MCA, increased histone acetylation levels in vivo. Ischemic preconditioning enhanced CBP recruitment and histone acetylation at the promoter of the neuroprotective gene gelsolin leading to increased gelsolin expression in neurons. Inhibition of CBP's HAT activity attenuated neuronal ischemic preconditioning. Taken together, our findings suggest that the levels of CBP and histone acetylation determine stroke outcome and are crucially associated with the induction of an ischemia-resistant state in neurons.

Indexed as

AcetylationAnimalsBrain IschemiaCerebral CortexCREB-Binding ProteinCurcuminDisease Models, AnimalGelsolinGene ExpressionGene Expression RegulationGene Knockdown TechniquesGenetic Predisposition to DiseaseHistonesMaleMiceMice, KnockoutCREB-Binding ProteinCurcuminGelsolinHistones

Identifiers

PMID24748101
PMCPMC3991684
OpenAlexW1984269521

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.