Evidence map›Paper›PMID 30063300›Full record

ArticleStem cells translational medicine2018

Dysregulation of Mesenchymal Stromal Cell Antioxidant Responses in Progressive Multiple Sclerosis.

Juliana Redondo, Pamela Sarkar, Kevin Kemp, Kate J Heesom, Alastair Wilkins, Neil J Scolding, Claire M Rice

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

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  15. Lung-resident mesenchymal stromal cells are tissue-specific regulators of lung homeostasis.American journal of physiology. Lung cellular and molecular physiology · 2020
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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

7 authors at 2 institutions in 1 country.

Juliana RedondoClinical Neuroscience, Translational Health Sciences, University of Bristol, Bristol, United Kingdom.
Pamela SarkarClinical Neuroscience, Translational Health Sciences, University of Bristol, Bristol, United Kingdom.
Kevin KempClinical Neuroscience, Translational Health Sciences, University of Bristol, Bristol, United Kingdom.
Kate J HeesomProteomics Facility, University of Bristol, Bristol, United Kingdom.
Alastair WilkinsClinical Neuroscience, Translational Health Sciences, University of Bristol, Bristol, United Kingdom.
Neil J ScoldingClinical Neuroscience, Translational Health Sciences, University of Bristol, Bristol, United Kingdom.
Claire M RiceClinical Neuroscience, Translational Health Sciences, University of Bristol, Bristol, United Kingdom.ORCID 0000-0002-9851-4426
University of Bristol · GBBristol Robotics Laboratory · GB

Funding

Medical Research Council MR/K004166/1Medical Research Council (UK) MR/K004166/1
6 · The paper itself

Abstract

The potential of autologous cell-based therapies including those using multipotent mesenchymal stromal cells (MSCs) is being investigated for multiple sclerosis (MS) and other neurological conditions. However, the phenotype of MSC in neurological diseases has not been fully characterized. We have previously shown that MSC isolated from patients with progressive MS (MS-MSC) have reduced expansion potential, premature senescence, and reduced neuroprotective potential in vitro. In view of the role of antioxidants in ageing and neuroprotection, we examined the antioxidant capacity of MS-MSC demonstrating that MS-MSC secretion of antioxidants superoxide dismutase 1 (SOD1) and glutathione S-transferase P (GSTP) is reduced and correlates negatively with the duration of progressive phase of MS. We confirmed reduced expression of SOD1 and GSTP by MS-MSC along with reduced activity of SOD and GST and, to examine the antioxidant capacity of MS-MSC under conditions of nitrosative stress, we established an in vitro cell survival assay using nitric oxide-induced cell death. MS-MSC displayed differential susceptibility to nitrosative stress with accelerated senescence and greater decline in expression of SOD1 and GSTP in keeping with reduced expression of master regulators of antioxidant responses nuclear factor erythroid 2-related factor 2 and peroxisome proliferator-activated receptor gamma coactivator 1-α. Our results are compatible with dysregulation of antioxidant responses in MS-MSC and have significant implications for development of autologous MSC-based therapies for MS, optimization of which may require that these functional deficits are reversed. Furthermore, improved understanding of the underlying mechanisms may yield novel insights into MS pathophysiology and biomarker identification. Stem Cells Translational Medicine 2018;7:748-758.

Indexed as

AntioxidantsBone Marrow CellsCellular SenescenceFemaleGlutathione TransferaseHumansMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiddle AgedMultiple SclerosisNF-E2-Related Factor 2Nitroso CompoundsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSuperoxide Dismutase-12,2'-(hydroxynitrosohydrazono)bis-ethanamineAntioxidantsGlutathione TransferaseNF-E2-Related Factor 2Nitroso CompoundsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanSuperoxide Dismutase-1AntioxidantsCell therapyMSCMultiple sclerosisNitrosative stress

Identifiers

PMID30063300
PMCPMC6186266
OpenAlexW2886181399

What OpenQuestion holds

Textmetadata
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.