Evidence map›Paper›PMID 24726920›Full record

ArticleExperimental eye research2014

All-trans-retinal induces Bax activation via DNA damage to mediate retinal cell apoptosis.

Osamu Sawada, Lindsay Perusek, Hideo Kohno, Scott J Howell, Akiko Maeda, Shigemi Matsuyama, Tadao Maeda

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Light as a Mediator of Acute and Chronic Retina Degeneration.Advances in experimental medicine and biology · 2025
    Review
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  18. The molecular aspects of absorption and metabolism of carotenoids and retinoids in vertebrates.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
  19. Article
  20. 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 3 institutions in 2 countries.

Osamu SawadaOphthalmology and Visual Sciences, School of Medicine, Case Western Reserve University, Adelbert Road 2085, Cleveland, OH 44106, USA; Ophthalmology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Lindsay PerusekOphthalmology and Visual Sciences, School of Medicine, Case Western Reserve University, Adelbert Road 2085, Cleveland, OH 44106, USA.
Hideo KohnoOphthalmology and Visual Sciences, School of Medicine, Case Western Reserve University, Adelbert Road 2085, Cleveland, OH 44106, USA; Ophthalmology, Jikei University School of Medicine, Minato-ku, Tokyo 105-8461, Japan.
Scott J HowellOphthalmology and Visual Sciences, School of Medicine, Case Western Reserve University, Adelbert Road 2085, Cleveland, OH 44106, USA.
Akiko MaedaOphthalmology and Visual Sciences, School of Medicine, Case Western Reserve University, Adelbert Road 2085, Cleveland, OH 44106, USA; Pharmacology, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Shigemi MatsuyamaPharmacology, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA; Medicine, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Tadao MaedaOphthalmology and Visual Sciences, School of Medicine, Case Western Reserve University, Adelbert Road 2085, Cleveland, OH 44106, USA; Pharmacology, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA. Electronic address: tadao.maeda@gmail.com.
Case Western Reserve University · USJikei University School of Medicine · JPShiga University of Medical Science · JP

Funding

TISSUE CULTURE AND HYBRIDOMA MODULEP30EY011373 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Irina A Pikuleva · 1997 to 2026
$17.7M
Pharmacological Treatment of Retinal DiseasesR24EY021126 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI PALCZEWSKI, KRZYSZTOF · 2010 to 2014
$12.8M
Reactive ocular aldehyde in degenerative retinal diseasesR01EY022658 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MAEDA, AKIKO · 2012 to 2016
$1.9M
Bax Activation Mechanism in the CytosolR01AG031903 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI MATSUYAMA, SHIGEMI · 2008 to 2012
$1.4M
Retinal degeneration diseases and the visual retinoid cycleK08EY019031 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MAEDA, AKIKO · 2008 to 2012
$430k
Genetics and Therapy of Age-related Retinal Dysfunction in A/J MiceK08EY019880 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MAEDA, TADAO · 2010 to 2013
$324k
NEI NIH HHS K08 EY019031NEI NIH HHS K08EY019031NEI NIH HHS K08 EY019880NEI NIH HHS KO8EY019880NEI NIH HHS P30 EY011373NEI NIH HHS P30EY011373NEI NIH HHS R01 EY022658NEI NIH HHS R01EY022658NEI NIH HHS R24 EY021126NEI NIH HHS R24EY021126NIA NIH HHS R01 AG031903NIA NIH HHS R01AG031903
6 · The paper itself

Abstract

The current study investigates the cellular events which trigger activation of proapoptotic Bcl-2-associated × protein (Bax) in retinal cell death induced by all-trans-retinal (atRAL). Cellular events which activate Bax, such as DNA damage by oxidative stress and phosphorylation of p53, were evaluated by immunochemical and biochemical methods using ARPE-19 cells, 661 W cells, cultured neural retinas and a retinal degeneration model, Abca4(-/-)Rdh8(-/-) mice. atRAL-induced Bax activation in cultured neural retinas was examined by pharmacological and genetic methods. Other Bax-related cellular events were also evaluated by pharmacological and biochemical methods. Production of 8-OHdG, a DNA damage indicator, and the phosphorylation of p53 at Ser46 were detected prior to Bax activation in ARPE-19 cells incubated with atRAL. Light exposure to Abca4(-/-)Rdh8(-/-) mice also caused the above mentioned events in conditions of short term intense light exposure and regular room lighting conditions. Incubation with Bax inhibiting peptide and deletion of the Bax gene partially protected retinal cells from atRAL toxicity in cultured neural retina. Necrosis was demonstrated not to be the main pathway in atRAL mediated cell death. Bcl-2-interacting mediator and Bcl-2 expression levels were not altered by atRAL in vitro. atRAL-induced oxidative stress results in DNA damage leading to the activation of Bax by phosphorylated p53. This cascade is closely associated with an apoptotic cell death mechanism rather than necrosis.

Indexed as

DNA Damage8-Hydroxy-2'-DeoxyguanosineAlcohol OxidoreductasesAnimalsApoptosisATP-Binding Cassette Transportersbcl-2-Associated X ProteinCell LineColorimetryDeoxyguanosineDisease Models, AnimalGene DeletionHumansImmunoblottingImmunohistochemistryL-Lactate Dehydrogenase8-Hydroxy-2'-DeoxyguanosineAbca4 protein, mouseAlcohol OxidoreductasesATP-Binding Cassette TransportersBAX protein, humanBax protein, mousebcl-2-Associated X ProteinDeoxyguanosineHSD17B6 protein, mouseL-Lactate DehydrogenaseRetinaldehydeTumor Suppressor Protein p53all-trans-retinalapoptosisBcl-2-associated × proteinDNA damageoxidative stressp53retinavisual cycle

Identifiers

PMID24726920
PMCPMC4083191
OpenAlexW2029502634

What OpenQuestion holds

Textmetadata
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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.