Evidence map›Paper›PMID 30423138›Full record

ArticleJournal of radiation research2019

Radiation resistance of normal human astrocytes: the role of non-homologous end joining DNA repair activity.

Michelle A Bylicky, Gregory P Mueller, Regina M Day

Open access · goldAbstract read
In one paragraph

Article in Journal of radiation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Multiple functions of p21 in cancer radiotherapy.Journal of cancer research and clinical oncology · 2021
    Review
  17. Long Noncoding RNAs Regulate the Radioresistance of Breast Cancer.Analytical cellular pathology (Amsterdam) · 2021
    Review
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Michelle A BylickyDepartment of Anatomy, Physiology, and Genetics, The Uniformed Services University of the Health Sciences, Jones Bridge Road, Bethesda, MD, USA.
Gregory P MuellerDepartment of Anatomy, Physiology, and Genetics, The Uniformed Services University of the Health Sciences, Jones Bridge Road, Bethesda, MD, USA.
Regina M DayDepartment of Pharmacology and Molecular Therapeutics, The Uniformed Services University of the Health Sciences, Jones Bridge Road, Bethesda, MD, USA.
Uniformed Services University of the Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy is a common modality for treatment of brain cancers, but it can induce long-term physiological and cognitive deficits. The responses of normal human brain cells to radiation is not well understood. Astrocytes have been shown to have a variety of protective mechanisms against oxidative stress and have been shown to protect neurons. We investigated the response of cultured normal human astrocytes (NHAs) to X-ray irradiation. Following exposure to 10 Gy X-irradiation, NHAs exhibited DNA damage as indicated by the formation of γ-H2AX foci. Western blotting showed that NHAs displayed a robust increase in expression of non-homologous end joining DNA repair enzymes within 15 min post-irradiation and increased expression of homologous recombination DNA repair enzymes ~2 h post-irradiation. The cell cycle checkpoint protein p21/waf1 was upregulated from 6-24 h, and then returned to baseline. Levels of DNA repair enzymes returned to basal ~48 h post-irradiation. NHAs re-entered the cell cycle and proliferation was observed at 6 days. In contrast, normal human mesenchymal stem cells (MSCs) failed to upregulate DNA repair enzymes and instead displayed sustained upregulation of p21/waf1, a cell cycle checkpoint marker for senescence. Ectopic overexpression of Ku70 was sufficient to protect MSCs from sustained upregulation of p21/waf1 induced by 10 Gy X-rays. These findings suggest that increased expression of Ku70 may be a key mechanism for the radioresistance of NHAs, preventing their accelerated senescence from high-dose radiation. These results may have implications for the development of novel targets for radiation countermeasure development.

Indexed as

DNA End-Joining RepairRadiation ToleranceApoptosisAstrocytesCell Cycle CheckpointsCell ProliferationCells, CulturedCellular SenescenceCyclin-Dependent Kinase Inhibitor p21CytoprotectionHEK293 CellsHomologous RecombinationHumansKu AutoantigenMesenchymal Stem CellsRadiation ExposureCyclin-Dependent Kinase Inhibitor p21Ku Autoantigen

Identifiers

PMID30423138
PMCPMC6373697
OpenAlexW2905325569

What OpenQuestion holds

Textmetadata
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.