Evidence map›Paper›PMID 34505865›Full record

ArticleInvestigative ophthalmology & visual science2021

Oxidative Stress Resistance 1 Gene Therapy Retards Neurodegeneration in the rd1 Mutant Mouse Model of Retinopathy.

Bhubanananda Sahu, Laura Moreno Leon, Wei Zhang, Nikita Puranik, Ramesh Periasamy, Hemant Khanna, Michael Volkert

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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

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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.

Bhubanananda SahuDepartment of Ophthalmology and Visual Science, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
Laura Moreno LeonDepartment of Ophthalmology and Visual Science, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
Wei ZhangDepartment of Ophthalmology and Visual Science, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
Nikita PuranikDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
Ramesh PeriasamyDepartment of Ophthalmology and Visual Science, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
Hemant KhannaDepartment of Ophthalmology and Visual Science, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
Michael VolkertNeuroNexus Institute, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
University of Massachusetts Chan Medical School · USNeuroNexus (United States) · US

Funding

Function of Ciliary Disease Protein Retinitis Pigmentosa GTPase Regulator (RPGR)R01EY022372 · NEI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI PAZOUR, GREGORY J · 2012 to 2020
$3.7M
NEI NIH HHS R01 EY022372
6 · The paper itself

Abstract

Purpose: Oxidative stress is a major factor underlying many neurodegenerative diseases. However, antioxidant therapy has had mixed results, possibly because of its indiscriminate activity. The purpose of our study was to determine if the human OXR1 (hOXR1) antioxidant regulatory gene could protect neurons from oxidative stress and delay photoreceptor cell death. Methods: The cone-like 661W cell line was transfected to stably express the hOXR1 gene. Oxidative stress was induced by the addition of hydrogen peroxide (H2O2). Intracellular levels of reactive oxygen species (ROS), caspase cleavage, and cellular resistance to oxidative stress were determined and compared between the control and hOXR1 cells. For in vivo analysis, AAV8-hOXR1 was injected subretinally into the rd1 mouse model of retinal degeneration. Functional and structural integrity of the photoreceptors were assessed using electroretinography (ERG), histology, and immunofluorescence analysis. Results: Expression of hOXR1 increased cellular resistance and reduced ROS levels and caspase cleavage in the 661W cell line after H2O2-induced oxidative stress. Subretinal injection of AAV8-hOXR1 in the rd1 mice improved their photoreceptor light response, expression and localization of photoreceptor-specific proteins, and delayed retinal degeneration. Conclusions: Our results suggest that OXR1 is a potential therapy candidate for retinal degeneration. Because OXR1 targets oxidative stress, a common feature of many retinal degenerative diseases, it should be of therapeutic value to multiple retinal degenerative diseases.

Indexed as

Gene Expression RegulationOxidative StressAnimalsCell DeathCells, CulturedDisease Models, AnimalGenetic TherapyHumansMiceMitochondrial ProteinsPhotoreceptor Cells, VertebrateReactive Oxygen SpeciesRetinaRetinal DegenerationRNAMitochondrial ProteinsOxr1 protein, mouseReactive Oxygen SpeciesRNA

Identifiers

PMID34505865
PMCPMC8434758
OpenAlexW3198534544

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.