Evidence map›Paper›PMID 32460314›Full record

ArticleInvestigative ophthalmology & visual science2020

Loss of High-Mobility Group Box 1 (HMGB1) Protein in Rods Accelerates Rod Photoreceptor Degeneration After Retinal Detachment.

Bing X Ross, Joanne Choi, Jingyu Yao, Heather M Hager, Steven F Abcouwer, David N Zacks

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Central Serous Chorioretinopathy Classification.Pharmaceuticals (Basel, Switzerland) · 2020
    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

6 authors at 3 institutions in 1 country.

Bing X Ross,.
Joanne Choi,.
Jingyu Yao,.
Heather M Hager,.
Steven F Abcouwer,.
David N Zacks,.
W.K. Kellogg Foundation · USMichigan United · USUniversity of Michigan–Ann Arbor · US

Funding

VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
Molecular Regulation of Photoreceptor Cell DeathR01EY020823 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABCOUWER, STEVEN F, ZACKS, DAVID N · 2010 to 2023
$5.0M
Vision Research Training Program - T32EY013934T32EY013934 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Patrice Elie Fort · 2002 to 2026
$4.2M
Inflammatory Resolution and Vascular Restoration in Diabetic RetinopathyR01EY029349 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABCOUWER, STEVEN F, ANTONETTI, DAVID · 2018 to 2022
$2.4M
NEI NIH HHS P30 EY007003NEI NIH HHS R01 EY020823NEI NIH HHS R01 EY029349NEI NIH HHS T32 EY013934
6 · The paper itself

Abstract

Purpose: Retinal detachment (RD) disrupts the nutritional support and oxygen delivery to photoreceptors (PRs), ultimately causing cell death. High-mobility group box 1 (HMGB1) can serve as an extracellular alarmin when released from stressed cells. PRs release HMGB1 after RD. The purpose of this study was to investigate the relationship between HMGB1 and PR survival after RD. Methods: Acute RD was created by injection of hyaluronic acid (1%) into the subretinal space in C57BL/6 mice and mice with a rhodopsin-Cre-mediated conditional knockout (cKO) of HMGB1 in rods (HMGB1ΔRod). Immunofluorescence (IF) in retinal sections was used to localize HMGB1, rhodopsin, and Iba-1 proteins. Optical coherence tomography and electroretinography were used to quantify retinal thickness and function, respectively. The morphology of the retina was assessed by hematoxylin and eosin. Results: HMGB1 protein was localized to the nuclei of all retinal neurons, including PRs, with cones staining more intensely than rods. HMGB1 protein was also found in the inner and outer segments of cones but not rods. Creation of RD caused a dramatic increase of HMGB1 protein IF in rods. cKO of HMGB1 in rods did not affect retinal structure or function. However, after RD, loss of rods and reduction in the thickness of the outer nuclear layer were significantly increased in the HMGB1ΔRod retinas as compared to the control. Interestingly, depletion of HMGB1 in rods did not affect the activation and mobilization of microglia/macrophages normally seen after RD. Conclusions: Increased HMGB1 expression in stressed rods may represent an intrinsic mechanism regulating their survival after RD.

Indexed as

AnimalsHMGB1 ProteinMiceMice, Inbred C57BLRetinal DegenerationRetinal DetachmentRetinal Rod Photoreceptor CellsTime FactorsHMGB1 ProteinHMGB1 protein, mouse

Identifiers

PMID32460314
PMCPMC7405795
OpenAlexW3028955911

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.