Evidence map›Paper›PMID 26788069›Full record

ArticleStem cells international2016

p53-Dependent Senescence in Mesenchymal Stem Cells under Chronic Normoxia Is Potentiated by Low-Dose γ-Irradiation.

Ines Höfig, Yashodhara Ingawale, Michael J Atkinson, Heidi Hertlein, Peter J Nelson, Michael Rosemann

Open access · goldAbstract read
In one paragraph

Article in Stem cells international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Epigenetic Alterations under Oxidative Stress in Stem Cells.Oxidative medicine and cellular longevity · 2022
    Review
  2. Mitochondria and autophagy in adult stem cells: proliferate or differentiate.Journal of muscle research and cell motility · 2020
    Article
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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

6 authors at 1 institution in 2 countries.

Ines HöfigInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, 85764 Neuherberg, Germany.ORCID 0000-0001-8319-8507
Yashodhara IngawaleInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, 85764 Neuherberg, Germany.
Michael J AtkinsonInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, 85764 Neuherberg, Germany; Chair of Radiation Biology, Technical University Munich, Ismaninger Straße 22, 81675 Munich, Germany.ORCID 0000-0003-3358-2089
Heidi HertleinInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, 85764 Neuherberg, Germany.
Peter J NelsonResearch Group Clinical Biochemistry, Medical Clinic and Polyclinic IV, Medical Center of the University of Munich, Schillerstraße 42, 80336 Munich, Germany.
Michael RosemannInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstraße 1, 85764 Neuherberg, Germany.ORCID 0000-0002-5855-065X
Center for Environmental Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are a source of adult multipotent cells important in tissue regeneration. Murine MSCs are known to proliferate poorly in vitro under normoxia. The aim of this study is to analyze the interaction of nonphysiological high oxygen and low-dose γ-irradiation onto growth, senescence, and DNA damage. Tri-potent bone marrow-derived MSCs from p53 wildtype and p53-/- mice were cultured under either 21% or 2% O2. Long-term observations revealed a decreasing ability of wildtype mMSCs to proliferate and form colonies under extended culture in normoxia. This was accompanied by increased senescence under normoxia but not associated with telomere shortening. After low-dose γ-irradiation, the normoxic wildtype cells further increased the level of senescence. The number of radiation-induced γH2AX DNA repair foci was higher in mMSCs kept under normoxia but not in p53-/- cells. P53-deficient MSCs additionally showed higher clonogeneity, lower senescence levels, and fewer γH2AX repair foci per cell as compared to their p53 wildtype counterparts irrespective of oxygen levels. These results reveal that oxygen levels together with γ-irradiation and p53 status are interconnected factors modulating growth capacity of BM MSCs in long-term culture. These efforts help to better understand and optimize handling of MSCs prior to their therapeutic use.

Identifiers

PMID26788069
PMCPMC4695678
OpenAlexW2237507851

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.