Evidence map›Paper›PMID 30008586›Full record

ArticleInternational journal of medical sciences2018

The replicative senescent mesenchymal stem / stromal cells defect in DNA damage response and anti-oxidative capacity.

Jin Yu, Jiazhong Shi, Yue Zhang, Yi Zhang, Yaqin Huang, Zhiwen Chen, Jin Yang

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

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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 2 institutions in 1 country.

Jin YuDepartment of Cell Biology, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Jiazhong ShiDepartment of Cell Biology, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Yue ZhangDepartment of Cell Biology, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Yi ZhangDepartment of Cell Biology, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Yaqin HuangDepartment of Cell Biology, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Zhiwen ChenUrology Institute of PLA, Southwest Hospital, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Jin YangDepartment of Cell Biology, Army Medical University (The Third Military Medical University), Chongqing 400038, China.
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replicative senescence and potential malignant transformation are great limitations in the clinical application of bone marrow-derived mesenchymal stem / stromal cells (MSCs). An abnormal DNA damage response may result in genomic instability, which is an integral component of aging and tumorigenesis. However, the effect of aging on the DNA damage response in MSCs is currently unknown. In the present study, we evaluated the DNA damage response induced by oxidative stress and DNA double-strand breaks in human bone marrow-derived MSCs. After long-term cell culture, replicative senescent MSCs (sMSCs) were characterized by a poor proliferation rate, high senescence-associated β-galactosidase activity, and enhanced expression of P53 and P16. Features of the DNA damage response in these sMSCs were then compared with those from early-passage MSCs. The sMSCs were more sensitive to hydrogen peroxide and bleomycin treatment with respect to cell viability and apoptosis induction. Combined with the comet assay, γH2AX foci characterization and reactive oxygen species detection were used to demonstrate that the antioxidant and DNA repair ability of sMSCs are attenuated. This result could be explained, at least in part, by the downregulation of anti-oxidation and DNA repair genes, including Cu/Zn-SOD, GPX, CAT, OGG1, XRCC1, Ku70, BRCA2 and XRCC4. In conclusion, MSCs aging is associated with a reduction in the DNA repair and anti-oxidative capacity.

Indexed as

Cellular SenescenceDNA DamageOxidative StressCell ProliferationCells, CulturedDNA-Binding ProteinsDNA RepairGene Expression RegulationHumansMesenchymal Stem CellsDNA-Binding ProteinsDNA damage responseDNA double-strand breaksmesenchymal stem cellsoxidative stressReplicative senescence

Identifiers

PMID30008586
PMCPMC6036081
OpenAlexW2807511021

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.