Evidence map›Paper›PMID 34406331›Full record

ArticleInvestigative ophthalmology & visual science2021

Sigma-1R Protects Retinal Ganglion Cells in Optic Nerve Crush Model for Glaucoma.

Linya Li, Shaoqing He, Yang Liu, Thomas Yorio, Dorette Z Ellis

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Optic nerve injury models under varying forces.International ophthalmology · 2023
    Article
  10. Defining the ligand-dependent proximatome of the sigma 1 receptor.Frontiers in cell and developmental biology · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. 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

5 authors at 3 institutions in 1 country.

Linya LiDepartment of Pharmacology and Neuroscience University of North Texas Health Science Center, Fort Worth, Texas, United States.
Shaoqing HeNorth Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas, United States.
Yang LiuDepartment of Pharmacology and Neuroscience University of North Texas Health Science Center, Fort Worth, Texas, United States.
Thomas YorioDepartment of Pharmacology and Neuroscience University of North Texas Health Science Center, Fort Worth, Texas, United States.
Dorette Z EllisDepartment of Pharmaceutical Sciences, University of North Texas Systems College of Pharmacy, University of North Texas Health Science Center, Fort Worth, Texas, United States.
University of North Texas Health Science Center · USSmith-Kettlewell Eye Research Institute · USUniversity of North Texas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: The purpose of this study was to determine the effects of the Sigma-1R (σ-1r) on retinal ganglion cell (RGC) survival following optic nerve crush (ONC) and the signaling mechanism involved in the σ-1r protection. Methods: The overall strategy was to induce injury by ONC and mitigate RGC death by increasing σ-1r expression and/or activate σ-1r activity in σ-1r K/O mice and wild type (WT) mice. AAV2-σ-1r vector was used to increase σ-1r expression and σ-1r agonist used to activate the σ-1r and RGCs were counted. Immunohistochemical and Western blot analysis determined phosphorylated (p)-c-Jun, c-Jun, and Caspase-3. Pattern electroretinography (PERG) determined RGC activity. Results: RGC counts and function were similar in pentazocine-treated WT mice when compared to untreated mice and in WT mice when compared with σ-1r K/O mice. Pentazocine-induced effects and the effects of σ-1r K/O were only observable after ONC. ONC resulted in decreased RGC counts and activity in both WT and σ-1r K/O mice, with σ-1r K/O mice experiencing significant decreases compared with WT mice. The σ-1r transgenic expression resulted in increased RGC counts and activity following ONC. In WT mice, treatment with σ-1r agonist pentazocine resulted in increased RGC counts and increased activity when compared with untreated WT mice. There were time-dependent increases in c-jun, p-c-jun, and caspase-3 expression in ONC mice that were mitigated with pentazocine-treatment. Conclusions: These findings suggest that the apoptotic pathway is involved in RGC losses seen in an ONC model. The σ-1r offers neuroprotection, as activation and/or transgenic expression of σ-1r attenuated the apoptotic pathway and restored RGCs number and function following ONC.

Indexed as

AnimalsApoptosisDisease Models, AnimalElectroretinographyGlaucomaMiceMice, Inbred C57BLMice, KnockoutNerve CrushOptic Nerve InjuriesReceptors, sigmaRetinal Ganglion CellsSigma-1 ReceptorSignal TransductionReceptors, sigmaSigma-1 Receptor

Identifiers

PMID34406331
PMCPMC8375012
OpenAlexW3193582984

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.