Evidence map›Paper›PMID 20716129›Full record

ArticleJournal of cellular and molecular medicine2011

Survival and function of mesenchymal stem cells (MSCs) depend on glucose to overcome exposure to long-term, severe and continuous hypoxia.

M Deschepper, K Oudina, B David, V Myrtil, C Collet, M Bensidhoum, D Logeart-Avramoglou, H Petite

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
3.1field-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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Can Hypoxic Conditioning Improve Bone Metabolism? A Systematic Review.International journal of environmental research and public health · 2019
    Pooled it
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  8. Graft ischemia post cell transplantation to the brain: Glucose deprivation as the primary driver of rapid cell death.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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9 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

M DeschepperLaboratory of Bio-engineering and Osteo-articular Biomaterial, University Denis Diderot, 10 Avenue de Verdun, Paris, France.
K Oudina
B David
V Myrtil
C Collet
M Bensidhoum
D Logeart-Avramoglou
H Petite
Université Paris Cité · FRHôpital Lariboisière · FRLaboratoire de Biologie, Bioingéniérie et Bioimagerie ostéoarticulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Use of mesenchymal stem cells (MSCs) has emerged as a potential new treatment for various diseases but has generated marginally successful results. A consistent finding of most studies is massive death of transplanted cells. The present study examined the respective roles of glucose and continuous severe hypoxia on MSC viability and function with respect to bone tissue engineering. We hereby demonstrate for the first time that MSCs survive exposure to long-term (12 days), severe (pO(2) < 1.5 mmHg) hypoxia, provided glucose is available. To this end, an in vitro model that mimics the hypoxic environment and cell-driven metabolic changes encountered by grafted sheep cells was established. In this model, the hallmarks of hypoxia (low pO(2) , hypoxia inducible factor-1α expression and anaerobic metabolism) were present. When conditions switched from hypoxic (low pO(2) ) to ischemic (low pO(2) and glucose depletion), MSCs exhibited shrinking, decreased cell viability and ATP content due to complete exhaustion of glucose at day 6; these results provided evidence that ischemia led to the observed massive cell death. Moreover, MSCs exposed to severe, continuous hypoxia, but without any glucose shortage, remained viable and maintained both their in vitro proliferative ability after simulation with blood reperfusion at day 12 and their in vivo osteogenic ability. These findings challenge the traditional view according to which severe hypoxia per se is responsible for the massive MSC death observed upon transplantation of these cells and provide evidence that MSCs are able to withstand exposure to severe, continuous hypoxia provided that a glucose supply is available.

Indexed as

Adenosine TriphosphateAnimalsCell HypoxiaCells, CulturedCell SurvivalGlucoseHypoxia-Inducible Factor 1, alpha SubunitIschemiaLactic AcidMesenchymal Stem CellsOxygenSheepTissue EngineeringTissue ScaffoldsAdenosine TriphosphateGlucoseHypoxia-Inducible Factor 1, alpha SubunitLactic AcidOxygen

Identifiers

PMID20716129
PMCPMC3823195
OpenAlexW2005484085

What Socratic 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 Socratic graph.