Evidence map›Paper›PMID 28118061›Full record

ArticleCell cycle (Georgetown, Tex.)2017

A comparison of radiation-induced mitochondrial damage between neural progenitor stem cells and differentiated cells.

Tsutomu Shimura, Megumi Sasatani, Hidehiko Kawai, Kenji Kamiya, Junya Kobayashi, Kenshi Komatsu, Naoki Kunugita

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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  8. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
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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

7 authors at 3 institutions in 1 country.

Tsutomu Shimuraa Department of Environmental Health , National Institute of Public Health , Wako , Saitama , Japan.
Megumi Sasatanib Department of Experimental Oncology , Research Center for Radiation Genome Medicine, Research Institute for Radiation Biology and Medicine (RIRBM), Hiroshima University , Hiroshima , Japan.
Hidehiko Kawaib Department of Experimental Oncology , Research Center for Radiation Genome Medicine, Research Institute for Radiation Biology and Medicine (RIRBM), Hiroshima University , Hiroshima , Japan.
Kenji Kamiyab Department of Experimental Oncology , Research Center for Radiation Genome Medicine, Research Institute for Radiation Biology and Medicine (RIRBM), Hiroshima University , Hiroshima , Japan.
Junya Kobayashic Department of Genome Dynamics , Radiation Biology Center, Kyoto University , Kyoto , Japan.
Kenshi Komatsuc Department of Genome Dynamics , Radiation Biology Center, Kyoto University , Kyoto , Japan.
Naoki Kunugitaa Department of Environmental Health , National Institute of Public Health , Wako , Saitama , Japan.
Hiroshima University · JPKyoto University · JPNational Institute of Public Health · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria play a key role in maintaining cellular homeostasis during stress responses, and mitochondrial dysfunction contributes to carcinogenesis, aging, and neurologic disease. We here investigated ionizing radiation (IR)-induced mitochondrial damage in human neural progenitor stem cells (NSCs), their differentiated counterparts and human normal fibroblasts. Long-term fractionated radiation (FR) with low doses of X-rays for 31 d enhanced mitochondrial activity as evident by elevated mitochondrial membrane potential (ΔΨm) and mitochondrial complex IV (cytochrome c oxidase) activity to fill the energy demands for the chronic DNA damage response in differentiated cells. Subsequent reduction of the antioxidant glutathione via continuous activation of mitochondrial oxidative phosphorylation caused oxidative stress and genomic instability in differentiated cells exposed to long-term FR. In contrast, long-term FR had no effect on the mitochondrial activity in NSCs. This cell type showed efficient DNA repair, no mitochondrial damage, and resistance to long-term FR. After high doses of acute single radiation (SR) (> 5 Gy), cell cycle arrest at the G2 phase was observed in NSCs and human fibroblasts. Under this condition, increase in mitochondria mass, mitochondrial DNA, and intracellular reactive oxygen species (ROS) levels were observed in the absence of enhanced mitochondrial activity. Consequently, cellular senescence was induced by high doses of SR in differentiated cells. In conclusion, we demonstrated that mitochondrial radiation responses differ according to the extent of DNA damage, duration of radiation exposure, and cell differentiation.

Indexed as

Cell Cycle CheckpointsCell DifferentiationCell NucleusCellular SenescenceDNA, MitochondrialDNA RepairDose-Response Relationship, RadiationFluorescent Antibody TechniqueG2 PhaseHistonesHumansMitochondriaNeural Stem CellsOxidation-ReductionOxidative PhosphorylationReactive Oxygen SpeciesDNA, MitochondrialH2AX protein, humanHistonesReactive Oxygen Specieslow-dose radiationmitochondrial damageneural stem cellsparkinROS

Identifiers

PMID28118061
PMCPMC5384592
OpenAlexW2582086885

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.