Evidence map›Paper›PMID 29668072›Full record

ArticleBrain pathology (Zurich, Switzerland)2019

A unique telomere DNA expansion phenotype in human retinal rod photoreceptors associated with aging and disease.

W Robert Bell, Alan K Meeker, Anthony Rizzo, Sumit Rajpara, Ian M Rosenthal, Miguel Flores Bellver, Silvia Aparicio Domingo, Xiufeng Zhong, John R Barber, Corinne E Joshu and 3 more

Abstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Development of High-Resolution Three-Dimensional-Printed Extracellular Matrix Scaffolds and Their Compatibility with Pluripotent Stem Cells and Early Retinal Cells.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
    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

13 authors.

W Robert BellDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Alan K MeekerDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Anthony RizzoDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Sumit RajparaDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Ian M RosenthalDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Miguel Flores BellverDepartments of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD.
Silvia Aparicio DomingoDepartments of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD.
Xiufeng ZhongDepartments of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD.
John R BarberDepartments of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
Corinne E JoshuDepartments of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD.
M Valeria Canto-SolerDepartments of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD.
Charles G EberhartDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Christopher M HeaphyDepartments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.ORCID 0000-0003-4264-1810

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have identified a discrete, focal telomere DNA expansion phenotype in the photoreceptor cell layer of normal, non-neoplastic human retinas. This phenotype is similar to that observed in a subset of human cancers, including a large fraction of tumors of the central nervous system, which maintain their telomeres via the non-telomerase-mediated alternative lengthening of telomeres (ALT) mechanism. We observed that these large, ultra-bright telomere DNA foci are restricted to the rod photoreceptors and are not observed in other cell types. Additionally, focus-positive rod cells are dispersed homogeneously throughout the posterior retinal photoreceptor cell layer and appear to be human-specific. We examined 108 normal human retinas obtained at autopsy from a wide range of ages. These large, ultra-bright telomere DNA foci were not observed in infants before 6 months of age; however, the prevalence of focus-positive rod cells dramatically increased throughout life. To investigate associations between this phenotype and retinal pathology, we assessed adult glaucoma (N = 29) and diabetic retinopathy (N = 38) cases. Focus-positive rod cells were prominent in these diseases. When compared to the normal group, after adjusting for age, logistic regression modeling revealed significantly increased odds of falling in the high category of focus-positive rod cells for glaucoma and diabetic retinopathy. In summary, we have identified a dramatic telomere alteration associated with aging and diseases affecting the retina.

Indexed as

Age FactorsAgingAnimalsDiabetic RetinopathyDNAFemaleGlaucomaHumansMalePhenotypePhotoreceptor Cells, VertebrateRetinaRetinal Rod Photoreceptor CellsTelomereTelomere HomeostasisDNAdiabetic retinopathyglaucomaretinarod photoreceptorstelomeres

Identifiers

PMID29668072
PMCPMC8028494

What OpenQuestion holds

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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.