Evidence map›Paper›PMID 27169377›Full record

ArticleMutation research. Genetic toxicology and environmental mutagenesis2016

Relationship between spontaneous γH2AX foci formation and progenitor functions in circulating hematopoietic stem and progenitor cells among atomic-bomb survivors.

Junko Kajimura, Seishi Kyoizumi, Yoshiko Kubo, Munechika Misumi, Kengo Yoshida, Tomonori Hayashi, Kazue Imai, Waka Ohishi, Kei Nakachi, Nan-Ping Weng and 5 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Mutation research. Genetic toxicology and environmental mutagenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Junko KajimuraDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan. Electronic address: kajimura@rerf.or.jp.
Seishi KyoizumiDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan.
Yoshiko KuboDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan.
Munechika MisumiDepartment of Statistics, Radiation Effects Research Foundation, Hiroshima, Japan.
Kengo YoshidaDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan.
Tomonori HayashiDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan.
Kazue ImaiDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan.
Waka OhishiDepartment of Clinical Studies, Radiation Effects Research Foundation, Hiroshima, Japan.
Kei NakachiDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan.
Nan-Ping WengLaboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Lauren F YoungDepartment of Medicine and Immunology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Jae-Hung ShiehDepartment of Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Malcolm A MooreDepartment of Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Marcel R M van den BrinkDepartment of Medicine and Immunology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Yoichiro KusunokiDepartments of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima, Japan. Electronic address: ykusunok@rerf.or.jp.
Radiation Effects Research Foundation · JPMemorial Sloan Kettering Cancer Center · USNational Institute on Aging · US

Funding

Mechanisms Of Transcriptional Regulation in Memory lymphocyte Response and AgingZIAAG000757 · NIA · NATIONAL INSTITUTE ON AGING · PI WENG, NAN-PING PETER · 2009 to 2025
$7.9M
Role of Telomere In Human Lymphocyte Function and AgingZIAAG000756 · NIA · NATIONAL INSTITUTE ON AGING · PI WENG, NAN-PING PETER · 2009 to 2025
$5.5M
Regulation and function of telomerase in T cellsZIAAG000112 · NIA · NATIONAL INSTITUTE ON AGING · PI WENG, NAN-PING PETER · 2009 to 2016
$1.2M
Molecular Mechanisms Of Memory T CellsZ01AG000757 · NIA · NATIONAL INSTITUTE ON AGING · PI WENG, NAN PING PETER · 1998 to 2008
$1.2M
Intramural NIH HHS Z01 AG000757Intramural NIH HHS ZIA AG000112
6 · The paper itself

Abstract

Accumulated DNA damage in hematopoietic stem cells is a primary mechanism of aging-associated dysfunction in human hematopoiesis. About 70 years ago, atomic-bomb (A-bomb) radiation induced DNA damage and functional decreases in the hematopoietic system of A-bomb survivors in a radiation dose-dependent manner. The peripheral blood cell populations then recovered to a normal range, but accompanying cells derived from hematopoietic stem cells still remain that bear molecular changes possibly caused by past radiation exposure and aging. In the present study, we evaluated radiation-related changes in the frequency of phosphorylated (Ser-139) H2AX (γH2AX) foci formation in circulating CD34-positive/lineage marker-negative (CD34+Lin-) hematopoietic stem and progenitor cells (HSPCs) among 226Hiroshima A-bomb survivors. An association between the frequency of γH2AX foci formation in HSPCs and the radiation dose was observed, but the γH2AX foci frequency was not significantly elevated by past radiation. We found a negative correlation between the frequency of γH2AX foci formation and the length of granulocyte telomeres. A negative interaction effect between the radiation dose and the frequency of γH2AX foci was suggested in a proportion of a subset of HSPCs as assessed by the cobblestone area-forming cell assay (CAFC), indicating that the self-renewability of HSPCs may decrease in survivors who were exposed to a higher radiation dose and who had more DNA damage in their HSPCs. Thus, although many years after radiation exposure and with advancing age, the effect of DNA damage on the self-renewability of HSPCs may be modified by A-bomb radiation exposure.

Indexed as

AgedAged, 80 and overAge FactorsCell DifferentiationDNA DamageHematopoietic Stem CellsHistonesHumansMiddle AgedStem CellsH2AX protein, humanHistonesAtomic-bombDNA damageHematopoietic stem and progenitor cellsSelf-renewabilityTelomere lengthγH2AX

Identifiers

PMID27169377
PMCPMC5152679
OpenAlexW2339085473

What OpenQuestion holds

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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.