Evidence map›Paper›PMID 31627491›Full record

ArticleInternational journal of molecular sciences2019

HDAC2 Regulates Glial Cell Activation in Ischemic Mouse Retina.

Mi Sun Sung, Hwan Heo, Gwang Hyeon Eom, So Young Kim, Helong Piao, Yue Guo, Sang Woo Park

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Glaucoma Animal Models beyond Chronic IOP Increase.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Changes in Class I and IIb HDACs by δ-Opioid in Chronic Rat Glaucoma Model.Investigative ophthalmology & visual science · 2020
    Article
  12. 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

7 authors at 2 institutions in 1 country.

Mi Sun SungDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea. sms84831@hanmail.net.ORCID 0000-0001-7512-7303
Hwan HeoDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea. intereye@empal.com.ORCID 0000-0003-2169-8770
Gwang Hyeon EomDepartment of Pharmacology, Chonnam National University Medical School, Hwasungun 58128, Korea. eomgh@chonnam.ac.kr.
So Young KimDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea. syou8246@naver.com.
Helong PiaoDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea. 179302143long@gmail.com.
Yue GuoDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea. gyhappypot@gmail.com.ORCID 0000-0002-7078-9663
Sang Woo ParkDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea. exo70@naver.com.
Chonnam National University Hospital · KRChonnam National University Hwasun Hospital · KR

Funding

Chonnam National University Hospital Biomedical Research Institute BCRI18019National Research Foundation of Korea NRF-2015R1D1A1A01059630National Research Foundation of Korea NRF-2017M3A9E8023019
6 · The paper itself

Abstract

The current study was undertaken to investigate whether histone deacetylases (HDACs) can modulate the viability of retinal ganglion cells (RGCs) and the activity of glial cells in a mouse model of retinal ischemia-reperfusion (IR) injury. C57BL/6J mice were subjected to constant elevation of intraocular pressure for 60 min to induce retinal IR injury. Expression of macroglial and microglial cell markers (GFAP and Iba1), hypoxia inducing factor (HIF)-1α, and histone acetylation was analyzed after IR injury. To investigate the role of HDACs in the activation of glial cells, overexpression of HDAC1 and HDAC2 isoforms was performed. To determine the effect of HDAC inhibition on RGC survival, trichostatin-A (TSA, 2.5 mg/kg) was injected intraperitoneally. After IR injury, retinal GFAP, Iba1, and HIF-1α were upregulated. Conversely, retinal histone acetylation was downregulated. Notably, adenoviral-induced overexpression of HDAC2 enhanced glial activation following IR injury, whereas overexpression of HDAC1 did not significantly affect glial activation. TSA treatment significantly increased RGC survival after IR injury. Our results suggest that increased activity of HDAC2 is closely related to glial activation in a mouse model of retinal IR injury and inhibition of HDACs by TSA showed neuroprotective potential in retinas with IR injuries.

Indexed as

AcetylationAnimalsDown-RegulationGlial Fibrillary Acidic ProteinHistone Deacetylase 2Histone Deacetylase InhibitorsHistonesHydroxamic AcidsHypoxia-Inducible Factor 1, alpha SubunitMiceNeurogliaReperfusion InjuryRetinaRetinal Ganglion CellsUp-RegulationGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseHdac2 protein, mouseHif1a protein, mouseHistone Deacetylase 2Histone Deacetylase InhibitorsHistonesHydroxamic AcidsHypoxia-Inducible Factor 1, alpha Subunittrichostatin Aglial cellhistone deacetylaseischemiaretinaretinal ganglion cell

Identifiers

PMID31627491
PMCPMC6829428
OpenAlexW2981271097

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.