Evidence map›Paper›PMID 27882538›Full record

ArticleBritish journal of pharmacology2017

Gene therapy with mesenchymal stem cells expressing IFN-ß ameliorates neuroinflammation in experimental models of multiple sclerosis.

C Marin-Bañasco, K Benabdellah, C Melero-Jerez, B Oliver, M J Pinto-Medel, I Hurtado-Guerrero, F de Castro, D Clemente, O Fernández, F Martin and 2 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-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

21 citing papers in PubMed, 47 citations in OpenAlex.

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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

12 authors at 6 institutions in 1 country.

C Marin-BañascoUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
K BenabdellahCell and Gene Therapy Group, Genomic Medicine Department, GENYO, Centre for Genomics and Oncological Research, Pfizer-University of Granada-Andalusian Regional Government, Granada, Spain.
C Melero-JerezGrupo de Neurobiología del Desarrollo-GNDe, Instituto Cajal-CSIC, 28002, Madrid, Spain.
B OliverUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
M J Pinto-MedelUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
I Hurtado-GuerreroUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
F de CastroGrupo de Neurobiología del Desarrollo-GNDe, Instituto Cajal-CSIC, 28002, Madrid, Spain.
D ClementeGrupo de Neuroinmuno-Reparación, Hospital Nacional de Parapléjicos, 45071, Toledo, Spain.
O FernándezUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
F MartinCell and Gene Therapy Group, Genomic Medicine Department, GENYO, Centre for Genomics and Oncological Research, Pfizer-University of Granada-Andalusian Regional Government, Granada, Spain.
L LeyvaUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
M SuardíazUnidad de Gestión Clínica Inter-centros de Neurociencias, Laboratorio de Investigación y Servicio de Neurología, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Spain.
Universidad de Málaga · ESHospital Nacional de Parapléjicos · ESInstituto de Investigación Biomédica de Málaga · ESPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ESSpanish Multiple Sclerosis Network · ESHospital Regional Universitario de Málaga · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeRecombinant IFN-ß is one of the first-line treatments in multiple sclerosis (MS), despite its lack of efficacy in some patients. In this context, mesenchymal stem cells (MSCs) represent a promising therapeutic alternative due to their immunomodulatory properties and multipotency. Moreover, by taking advantage of their pathotropism, these cells can be genetically modified to be used as carriers for delivering or secreting therapeutic drugs into injured tissues. Here, we report the therapeutic effect of systemic delivery of adipose-derived MSCs (AdMSCs), transduced with the IFN-β gene, into mice with experimental autoimmune encephalomyelitis (EAE). EXPERIMENTAL APPROACH: Relapsing-remitting and chronic progressive EAE were induced in mice. Cells were injected i.v. Disease severity, inflammation and tissue damage were assessed clinically, by flow cytometry of spleens and histopathological evaluation of the CNS respectively. KEY

resultsGenetic engineering did not modify the biological characteristics of these AdMSCs (morphology, growth rate, immunophenotype and multipotency). Furthermore, the transduction of IFN-ß to AdMSCs maintained and, in some cases, enhanced the functional properties of AdMSCs by ameliorating the symptoms of MS in EAE models and by decreasing indications of peripheral and central neuro-inflammation. CONCLUSION AND IMPLICATIONS: Gene therapy was found to be more effective than cell therapy in ameliorating several clinical parameters in both EAE models, presumably due to the continuous expression of IFN-β. Furthermore, it has significant advantages over AdMSC therapy, and also over systemic IFN-ß treatment, by providing long-term expression of the cytokine at therapeutic concentrations and reducing the frequency of injections, while minimizing dose-limiting side effects.

Indexed as

Adipose TissueAnimalsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleFlow CytometryGenetic TherapyInterferon-betaMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingSeverity of Illness IndexInterferon-beta

Identifiers

PMID27882538
PMCPMC5241389
OpenAlexW2554214255

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.