Evidence map›Paper›PMID 24069165›Full record

ArticlePloS one2013

Therapeutic potential of mesenchymal stromal cells and MSC conditioned medium in Amyotrophic Lateral Sclerosis (ALS)--in vitro evidence from primary motor neuron cultures, NSC-34 cells, astrocytes and microglia.

Hui Sun, Karelle Bénardais, Nancy Stanslowsky, Nadine Thau-Habermann, Niko Hensel, Dongya Huang, Peter Claus, Reinhard Dengler, Martin Stangel, Susanne Petri

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
4.5field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

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  8. Current neuropharmacology · 2022
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  9. Nitric oxide modulation in neuroinflammation and the role of mesenchymal stem cells.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  10. Review
  11. Adipose-derived stem cells protect motor neurons and reduce glial activation in bothMolecular therapy. Methods & clinical development · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

10 authors at 3 institutions in 2 countries.

Hui SunDepartment of Neurology, Hannover Medical School, Hannover, Germany ; Center for Systems Neuroscience, Hannover, Germany.
Karelle Bénardais
Nancy Stanslowsky
Nadine Thau-Habermann
Niko Hensel
Dongya Huang
Peter Claus
Reinhard Dengler
Martin Stangel
Susanne Petri
Medizinische Hochschule Hannover · DEIntegrierte Forschungs- und Behandlungszentren · DEShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Administration of mesenchymal stromal cells (MSC) improves functional outcome in the SOD1G93A mouse model of the degenerative motor neuron disorder amyotrophic lateral sclerosis (ALS) as well as in models of other neurological disorders. We have now investigated the effect of the interaction between MSC and motor neurons (derived from both non-transgenic and mutant SOD1G93A transgenic mice), NSC-34 cells and glial cells (astrocytes, microglia) (derived again from both non-transgenic and mutant SOD1G93A ALS transgenic mice) in vitro. In primary motor neurons, NSC-34 cells and astrocytes, MSC conditioned medium (MSC CM) attenuated staurosporine (STS) - induced apoptosis in a concentration-dependent manner. Studying MSC CM-induced expression of neurotrophic factors in astrocytes and NSC-34 cells, we found that glial cell line-derived neurotrophic factor (GDNF) and ciliary neurotrophic factor (CNTF) gene expression in astrocytes were significantly enhanced by MSC CM, with differential responses of non-transgenic and mutant astrocytes. Expression of Vascular Endothelial Growth Factor (VEGF) in NSC-34 cells was significantly upregulated upon MSC CM-treatment. MSC CM significantly reduced the expression of the cytokines TNFα and IL-6 and iNOS both in transgenic and non-transgenic astrocytes. Gene expression of the neuroprotective chemokine Fractalkine (CX3CL1) was also upregulated in mutant SOD1G93A transgenic astrocytes by MSC CM treatment. Correspondingly, MSC CM increased the respective receptor, CX3CR1, in mutant SOD1G93A transgenic microglia. Our data demonstrate that MSC modulate motor neuronal and glial response to apoptosis and inflammation. MSC therefore represent an interesting candidate for further preclinical and clinical evaluation in ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsApoptosisAstrocytesCells, CulturedChemokine CX3CL1Ciliary Neurotrophic FactorCulture Media, ConditionedGlial Cell Line-Derived Neurotrophic FactorsHumansMesenchymal Stem CellsMiceMicrogliaMotor NeuronsStaurosporineChemokine CX3CL1Ciliary Neurotrophic FactorCulture Media, ConditionedGlial Cell Line-Derived Neurotrophic FactorsStaurosporine

Identifiers

PMID24069165
PMCPMC3771979
OpenAlexW2149751073

What OpenQuestion holds

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LicenceCC BY
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.