Evidence map›Paper›PMID 23088254›Full record

ArticleAntioxidants & redox signaling2013

H2O2 accumulation mediates differentiation capacity alteration, but not proliferative decline, in senescent human fetal mesenchymal stem cells.

Pai-Jiun Ho, Men-Luh Yen, Bo-Chung Tang, Chiung-Tong Chen, B Linju Yen

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

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  12. A Rapid and Highly PredictiveFrontiers in cell and developmental biology · 2020
    Article
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  14. Review
  15. Production of Mesenchymal Stem Cells Through Stem Cell Reprogramming.International journal of molecular sciences · 2019
    Review
  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

5 authors.

Pai-Jiun HoRegenerative Medicine Research Group, Institute of Cellular and System Medicine ICSM, National Health Research Institute NHRI, Zhunan 350, Taiwan.
Men-Luh Yen
Bo-Chung Tang
Chiung-Tong Chen
B Linju Yen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsMesenchymal stem cells (MSCs) with multilineage differentiation capacity and immunomodulatory properties are novel sources for cell therapy. However, in vitro expansion of these rare somatic stem cells leads to senescence, resulting in declines of differentiation and proliferative capacities. We therefore investigated the mechanisms mediating senescence in human fetal MSCs termed placenta-derived multipotent cells (PDMCs).

resultsLong-term cultured PDMCs underwent senescence, with increased levels of hydrogen peroxide (H2O2; a reactive oxygen species), positive β-galactosidase staining, decreased sirtuin-1 expression, increased p21 expression, and cell cycle arrest at the G0/G1 phase. Senescent PDMCs also showed decreased osteogenic capacity. Mechanistically, increased p21 expression and proliferative decline were not due to elevated H2O2 levels nor mediated by p53. Instead, inhibition of protein kinase C (PKC)-α and -β in senescent PDMCs decreased p21 expression and reversed cell cycle arrest. H2O2 was involved in the alteration of differentiation potential, since scavenging of H2O2 restored expression of c-MAF, an osteogenic and age-sensitive transcription factor, and osteogenic capacity in senescent PDMCs. INNOVATION: Our findings not only show the effects of senescence on MSCs, but also reveal mechanisms involved in mediating decreased proliferation and differentiation capacity. Moreover, targeting increased levels of H2O2 associated with senescence may reverse the decreased osteogenic capacity of senescent MSCs.

conclusionOur study suggests that the two biological consequences of senescence, differentiation alteration, and proliferative decline, in fetal MSCs are distinctly regulated by the H2O2-c-MAF and PKC-p21 pathways, respectively.

Indexed as

Cell DifferentiationCellular SenescenceAdipogenesisCell Cycle CheckpointsCell LineageCell ProliferationCells, CulturedEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleFetal Stem CellsHumansHydrogen PeroxideMesenchymal Stem CellsPlacentaPregnancyExtracellular Signal-Regulated MAP KinasesHydrogen PeroxideProtein Kinase CProto-Oncogene Proteins c-mafProto-Oncogene Proteins p21(ras)Tumor Suppressor Protein p53

Identifiers

PMID23088254
PMCPMC3624695

What OpenQuestion holds

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Registered trials

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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.