Evidence map›Paper›PMID 28300292›Full record

ArticleJournal of cellular physiology2018

HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals.

Josef Večeřa, Eva Bártová, Jana Krejčí, Soňa Legartová, Denisa Komůrková, Jana Rudá-Kučerová, Tibor Štark, Eva Dražanová, Tomáš Kašpárek, Alexandra Šulcová and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

17 authors at 7 institutions in 5 countries.

Josef VečeřaFaculty of Science, Department of Experimental Biology, Masaryk University, Brno, Czech Republic.
Eva BártováInstitute of Biophysics of the Czech Academy of Sciences, v.v.i., Brno, Czech Republic.ORCID http://orcid.org/0000-0003-1299-0470
Jana KrejčíInstitute of Biophysics of the Czech Academy of Sciences, v.v.i., Brno, Czech Republic.
Soňa LegartováInstitute of Biophysics of the Czech Academy of Sciences, v.v.i., Brno, Czech Republic.
Denisa KomůrkováInstitute of Biophysics of the Czech Academy of Sciences, v.v.i., Brno, Czech Republic.
Jana Rudá-KučerováFaculty of Medicine, Department of Pharmacology, Masaryk University, Brno, Czech Republic.
Tibor ŠtarkFaculty of Medicine, Department of Pharmacology, Masaryk University, Brno, Czech Republic.
Eva DražanováFaculty of Medicine, Department of Pharmacology, Masaryk University, Brno, Czech Republic.
Tomáš KašpárekBehavioral and Social Neuroscience Group, CEITEC-Central European Institute of Technology, Masaryk University, Brno, Czech Republic.
Alexandra ŠulcováBehavioral and Social Neuroscience Group, CEITEC-Central European Institute of Technology, Masaryk University, Brno, Czech Republic.
Frank J DekkerChemical and Pharmaceutical Biology, University of Groningen, Groningen, The Netherlands.
Wiktor SzymanskiDepartment of Radiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Christian SeiserMax F. Perutz Laboratories, Vienna Biocenter (VBC), Vienna, Austria.
Georg WeitzerMax F. Perutz Laboratories, Vienna Biocenter (VBC), Vienna, Austria.
Raphael MechoulamFaculty of Medicine, Institute for Drug Research, Hebrew University of Jerusalem, Jerusalem, Israel.
Vincenzo MicaleBehavioral and Social Neuroscience Group, CEITEC-Central European Institute of Technology, Masaryk University, Brno, Czech Republic.
Stanislav KozubekFaculty of Science, Department of Experimental Biology, Masaryk University, Brno, Czech Republic.
Masaryk University · CZCzech Academy of Sciences · CZCentral European Institute of Technology · CZMax Perutz Labs · ATHebrew University of Jerusalem · ILUniversity Medical Center Groningen · NLUniversity of Groningen · NL

Funding

Austrian Science Fund FWF P 18659European Research Council 309782
6 · The paper itself

Abstract

Although histone acetylation is one of the most widely studied epigenetic modifications, there is still a lack of information regarding how the acetylome is regulated during brain development and pathophysiological processes. We demonstrate that the embryonic brain (E15) is characterized by an increase in H3K9 acetylation as well as decreases in the levels of HDAC1 and HDAC3. Moreover, experimental induction of H3K9 hyperacetylation led to the overexpression of NCAM in the embryonic cortex and depletion of Sox2 in the subventricular ependyma, which mimicked the differentiation processes. Inducing differentiation in HDAC1-deficient mouse ESCs resulted in early H3K9 deacetylation, Sox2 downregulation, and enhanced astrogliogenesis, whereas neuro-differentiation was almost suppressed. Neuro-differentiation of (wt) ESCs was characterized by H3K9 hyperacetylation that was associated with HDAC1 and HDAC3 depletion. Conversely, the hippocampi of schizophrenia-like animals showed H3K9 deacetylation that was regulated by an increase in both HDAC1 and HDAC3. The hippocampi of schizophrenia-like brains that were treated with the cannabinoid receptor-1 inverse antagonist AM251 expressed H3K9ac at the level observed in normal brains. Together, the results indicate that co-regulation of H3K9ac by HDAC1 and HDAC3 is important to both embryonic brain development and neuro-differentiation as well as the pathophysiology of a schizophrenia-like phenotype.

Indexed as

NeurogenesisAcetylationAnimalsAntipsychotic AgentsBrainCannabinoid Receptor AntagonistsDisease Models, AnimalEpigenesis, GeneticGene Expression Regulation, DevelopmentalGestational AgeHistone Deacetylase 1Histone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesMethylazoxymethanol AcetateAntipsychotic AgentsCannabinoid Receptor AntagonistsCnr1 protein, ratHdac1 protein, mouseHdac1 protein, ratHistone Deacetylase 1Histone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesMethylazoxymethanol AcetateNeural Cell Adhesion MoleculesReceptor, Cannabinoid, CB1Sox2 protein, mouseSOXB1 Transcription FactorsacetylomeH3K9 acetylationHDACsmouse neurogenesisschizophrenia

Identifiers

PMID28300292
PMCPMC7615847
OpenAlexW2596475028

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.