Evidence map›Paper›PMID 25619736›Full record

ArticleJournal of cellular and molecular medicine2015

Persistent DNA damage-induced premature senescence alters the functional features of human bone marrow mesenchymal stem cells.

Valentina Minieri, Silvia Saviozzi, Giovanna Gambarotta, Marco Lo Iacono, Lisa Accomasso, Elisa Cibrario Rocchietti, Clara Gallina, Valentina Turinetto, Claudia Giachino

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. The Mechanism of Icariin in Regulating BMSCs for Treating Osteoporosis: A Review.Endocrine, metabolic & immune disorders drug targets · 2026
    Review
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  18. Article
  19. Review
  20. Dual Role of Autophagy in Regulation of Mesenchymal Stem Cell Senescence.Frontiers in cell and developmental biology · 2020
    Review
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

9 authors at 1 institution in 1 country.

Valentina MinieriDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Turin, Italy.
Silvia Saviozzi
Giovanna Gambarotta
Marco Lo Iacono
Lisa Accomasso
Elisa Cibrario Rocchietti
Clara Gallina
Valentina Turinetto
Claudia Giachino
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human mesenchymal stem cells (hMSCs) are adult multipotent stem cells located in various tissues, including the bone marrow. In contrast to terminally differentiated somatic cells, adult stem cells must persist and function throughout life to ensure tissue homeostasis and repair. For this reason, they must be equipped with DNA damage responses able to maintain genomic integrity while ensuring their lifelong persistence. Evaluation of hMSC response to genotoxic insults is of great interest considering both their therapeutic potential and their physiological functions. This study aimed to investigate the response of human bone marrow MSCs to the genotoxic agent Actinomycin D (ActD), a well-known anti-tumour drug. We report that hMSCs react by undergoing premature senescence driven by a persistent DNA damage response activation, as hallmarked by inhibition of DNA synthesis, p21 and p16 protein expression, marked Senescent Associated β-galactosidase activity and enlarged γH2AX foci co-localizing with 53BP1 protein. Senescent hMSCs overexpress several senescence-associated secretory phenotype (SASP) genes and promote motility of lung tumour and osteosarcoma cell lines in vitro. Our findings disclose a multifaceted consequence of ActD treatment on hMSCs that on the one hand helps to preserve this stem cell pool and prevents damaged cells from undergoing neoplastic transformation, and on the other hand alters their functional effects on the surrounding tissue microenvironment in a way that might worsen their tumour-promoting behaviour.

Indexed as

DNA DamageAntibiotics, Antineoplasticbeta-GalactosidaseCell DifferentiationCell Line, TumorCells, CulturedCell SurvivalCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DactinomycinDNAGene ExpressionHistonesHumansImmunoblottingAntibiotics, Antineoplasticbeta-GalactosidaseCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DactinomycinDNAH2AX protein, humanHistonesInterleukin-6Interleukin-8Intracellular Signaling Peptides and ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1actinomycin DDNA damagemesenchymal stem cellsenescence-associated secretory phenotypestress-induced premature senescence

Identifiers

PMID25619736
PMCPMC4395188
OpenAlexW1977468021

What OpenQuestion holds

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LicenceCC BY
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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.