Evidence map›Paper›PMID 31653972›Full record

ArticleScientific reports2019

Depletion of Mitochondrial DNA in Differentiated Retinal Pigment Epithelial Cells.

Xinqian Hu, Melissa A Calton, Shibo Tang, Douglas Vollrath

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
1.8field-weighted citation impact, top 15% 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. Article
  2. Review
  3. Article
  4. Metabolic Phenotyping of Healthy and Diseased Human RPE Cells.Investigative ophthalmology & visual science · 2024
    Article
  5. Article
  6. Article
  7. Retinal Toxicity Induced by Chemical Agents.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. The Emerging Role of Senescence in Ocular Disease.Oxidative medicine and cellular longevity · 2020
    Review
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

4 authors at 3 institutions in 2 countries.

Xinqian HuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, 510060, China. xinqianhu@hotmail.com.
Melissa A CaltonDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Shibo TangAIER School of Ophthalmology, Central South University, Changsha, China.
Douglas VollrathDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Stanford University · USChinese Academy of Sciences · CNSun Yat-sen University · CN

Funding

RPE Energy Metabolism and Cell PhenotypeR01EY025790 · NEI · STANFORD UNIVERSITY · PI VOLLRATH, DOUGLAS E. · 2016 to 2021
$2.4M
Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) No.EY025790NEI NIH HHS R01 EY025790
6 · The paper itself

Abstract

We investigated the effects of treating differentiated retinal pigment epithelial (RPE) cells with didanosine (ddI), which is associated with retinopathy in individuals with HIV/AIDS. We hypothesized that such treatment would cause depletion of mitochondrial DNA and provide insight into the consequences of degradation of RPE mitochondrial function in aging and disease. Treatment of differentiated ARPE-19 or human primary RPE cells with 200 µM ddI for 6-24 days was not cytotoxic but caused up to 60% depletion of mitochondrial DNA, and a similar reduction in mitochondrial membrane potential and NDUFA9 protein abundance. Mitochondrial DNA-depleted RPE cells demonstrated enhanced aerobic glycolysis by extracellular flux analysis, increased AMP kinase activation, reduced mTOR activity, and increased resistance to cell death in response to treatment with the oxidant, sodium iodate. We conclude that ddI-mediated mitochondrial DNA depletion promotes a glycolytic shift in differentiated RPE cells and enhances resistance to oxidative damage. Our use of ddI treatment to induce progressive depletion of mitochondrial DNA in differentiated human RPE cells should be widely applicable for other studies aimed at understanding RPE mitochondrial dysfunction in aging and disease.

Indexed as

Adenylate KinaseCell DifferentiationCell LineDidanosineDNA, MitochondrialEpithelial CellsGlycolysisHumansMechanistic Target of Rapamycin Complex 1Membrane Potential, MitochondrialMitochondriaOxidative StressRetinal Pigment EpitheliumAdenylate KinaseDidanosineDNA, MitochondrialMechanistic Target of Rapamycin Complex 1

Identifiers

PMID31653972
PMCPMC6814719
OpenAlexW2981477879

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.