Evidence map›Paper›PMID 29478902›Full record

ArticleStem cell reports2018

TGF-β Signaling Accelerates Senescence of Human Bone-Derived CD271 and SSEA-4 Double-Positive Mesenchymal Stromal Cells.

Hiroshi Kawamura, Ryusuke Nakatsuka, Yoshikazu Matsuoka, Keisuke Sumide, Tatsuya Fujioka, Hiroaki Asano, Hirokazu Iida, Yoshiaki Sonoda

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
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  4. ZNF384-Driven Fibulin-1 Exacerbates Vascular Stiffness via TGF-β/Smad3-Mediated Senescence and Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
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  12. Article
  13. Mesenchymal Stromal Cells as a Driver of Inflammaging.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. 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

8 authors at 2 institutions in 1 country.

Hiroshi KawamuraDepartment of Stem Cell Biology and Regenerative Medicine, Graduate School of Medical Science, Kansai Medical University, Hirakata, Osaka 573-1010, Japan; Department of Orthopaedic Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
Ryusuke NakatsukaDepartment of Stem Cell Biology and Regenerative Medicine, Graduate School of Medical Science, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Yoshikazu MatsuokaDepartment of Stem Cell Biology and Regenerative Medicine, Graduate School of Medical Science, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Keisuke SumideDepartment of Stem Cell Biology and Regenerative Medicine, Graduate School of Medical Science, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Tatsuya FujiokaDepartment of Stem Cell Biology and Regenerative Medicine, Graduate School of Medical Science, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Hiroaki AsanoSchool of Nursing, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hirokazu IidaDepartment of Orthopaedic Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
Yoshiaki SonodaDepartment of Stem Cell Biology and Regenerative Medicine, Graduate School of Medical Science, Kansai Medical University, Hirakata, Osaka 573-1010, Japan. Electronic address: sonoda@hirakata.kmu.ac.jp.
Kansai Medical University · JPKyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is generally thought that the proliferative capacity and differentiation potential of somatic stem cells, including mesenchymal stromal/stem cells (MSCs) and hematopoietic stem cells, decline with age. We investigated the effects of aging on human bone-derived MSCs expressing CD271 and SSEA-4 (double-positive MSCs [DPMSCs]). The percentages of DPMSCs in bone tissue decreased significantly with age. The DPMSCs from elderly patients (old DPMSCs) showed cellular senescence, which was evidenced by low growth potential, high senescence-associated β-galactosidase activity, and elevated p16 and p21 CDK inhibitor levels. Moreover, old DPMSCs showed weak osteogenic differentiation potential and less hematopoiesis-supporting activity in comparison with young DPMSCs. Interestingly, the addition of transforming growth factor β2 (TGF-β2) induced cellular senescence in young DPMSCs. With the exception of the adipogenic differentiation potential, all of the aging phenomena observed in old DPMSCs were reversed by the addition of anti-TGF-β antibodies. These results suggest that, in part, old DPMSCs accelerate cellular senescence through TGF-β signaling.

Indexed as

AdipogenesisAdultAged, 80 and overAgingbeta-GalactosidaseBone Marrow CellsCell DifferentiationCell ProliferationCells, CulturedCellular SenescenceFemaleHematopoietic Stem CellsHumansMaleMesenchymal Stem CellsNerve Tissue Proteinsbeta-GalactosidaseNerve Tissue ProteinsNGFR protein, humanReceptors, Nerve Growth Factorstage-specific embryonic antigen-4Stage-Specific Embryonic AntigensTransforming Growth Factor betaagingHSChuman boneMSCrejuvenationsenescenceTGF-β

Identifiers

PMID29478902
PMCPMC5918367
OpenAlexW2788920070

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.