Evidence map›Paper›PMID 20504333›Full record

ArticleBMC neuroscience2010

Histone H4 deacetylation plays a critical role in early gene silencing during neuronal apoptosis.

Heather R Pelzel, Cassandra L Schlamp, Robert W Nickells

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Epigenetics in Glaucoma.Medicina (Kaunas, Lithuania) · 2024
    Review
  8. Article
  9. Dysregulation of histone deacetylases in ocular diseases.Archives of pharmacal research · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Aging Effects on Optic Nerve Neurodegeneration.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Epigenetic Regulation of Optic Nerve Development, Protection, and Repair.International journal of molecular sciences · 2022
    Review
  18. Monocyte-derived SDF1 supports optic nerve regeneration and alters retinal ganglion cells' response to Pten deletion.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  19. Article
  20. Review

28 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Heather R PelzelDepartment of Biomolecular Chemistry, University of Wisconsin, 1300 University Ave, 6671 MSC, Madison, WI 53706, USA.
Cassandra L Schlamp
Robert W Nickells
University of Wisconsin–Madison · USUniversity of Wisconsin System · US

Funding

UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
The molecular mechanism of retinal ganglion cell deathR01EY012223 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI NICKELLS, ROBERT W · 2005 to 2017
$6.3M
NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY012223NEI NIH HHS R01 EY12223
6 · The paper itself

Abstract

backgroundSilencing of normal gene expression occurs early in the apoptosis of neurons, well before the cell is committed to the death pathway, and has been extensively characterized in injured retinal ganglion cells. The causative mechanism of this widespread change in gene expression is unknown. We investigated whether an epigenetic change in active chromatin, specifically histone H4 deacetylation, was an underlying mechanism of gene silencing in apoptotic retinal ganglion cells (RGCs) following an acute injury to the optic nerve.

resultsHistone deacetylase 3 (HDAC3) translocates to the nuclei of dying cells shortly after lesion of the optic nerve and is associated with an increase in nuclear HDAC activity and widespread histone deacetylation. H4 in promoters of representative genes was rapidly and indiscriminately deacetylated, regardless of the gene examined. As apoptosis progressed, H4 of silenced genes remained deacetylated, while H4 of newly activated genes regained, or even increased, its acetylated state. Inhibition of retinal HDAC activity with trichostatin A (TSA) was able to both preserve the expression of a representative RGC-specific gene and attenuate cell loss in response to optic nerve damage.

conclusionsThese data indicate that histone deacetylation plays a central role in transcriptional dysregulation in dying RGCs. The data also suggests that HDAC3, in particular, may feature heavily in apoptotic gene silencing.

Indexed as

AcetylationAnimalsApoptosisBlotting, WesternChromatin ImmunoprecipitationFluorescent Antibody TechniqueGene SilencingHistone Deacetylase 3Histone DeacetylasesHistonesMiceOptic Nerve InjuriesRetinal Ganglion CellsReverse Transcriptase Polymerase Chain ReactionHistone Deacetylase 3Histone DeacetylasesHistones

Identifiers

PMID20504333
PMCPMC2886060
OpenAlexW2159404239

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.