Evidence map›Paper›PMID 34202139›Full record

ArticleInternational journal of molecular sciences2021

Extracellular Vesicles Are More Potent Than Adipose Mesenchymal Stromal Cells to Exert an Anti-Fibrotic Effect in an In Vitro Model of Systemic Sclerosis.

Pauline Rozier, Marie Maumus, Claire Bony, Alexandre Thibault Jacques Maria, Florence Sabatier, Christian Jorgensen, Philippe Guilpain, Danièle Noël

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  10. [Expression and significance of ferroptosis marker 4-HNE inBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024
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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

8 authors at 1 institution in 1 country.

Pauline RozierINSERM U1183, Hôpital Saint-Eloi, IRMB, University of Montpellier, 80 Avenue Augustin Fliche, CEDEX 5, 34295 Montpellier, France.
Marie MaumusINSERM U1183, Hôpital Saint-Eloi, IRMB, University of Montpellier, 80 Avenue Augustin Fliche, CEDEX 5, 34295 Montpellier, France.
Claire BonyINSERM U1183, Hôpital Saint-Eloi, IRMB, University of Montpellier, 80 Avenue Augustin Fliche, CEDEX 5, 34295 Montpellier, France.
Alexandre Thibault Jacques MariaDepartment of Internal Medicine, Multi-Organic Diseases, CHU, 34295 Montpellier, France.
Florence SabatierINSERM, INRA, C2VN, Aix Marseille University, 13005 Marseille, France.
Christian JorgensenINSERM U1183, Hôpital Saint-Eloi, IRMB, University of Montpellier, 80 Avenue Augustin Fliche, CEDEX 5, 34295 Montpellier, France.
Philippe GuilpainINSERM U1183, Hôpital Saint-Eloi, IRMB, University of Montpellier, 80 Avenue Augustin Fliche, CEDEX 5, 34295 Montpellier, France.
Danièle NoëlINSERM U1183, Hôpital Saint-Eloi, IRMB, University of Montpellier, 80 Avenue Augustin Fliche, CEDEX 5, 34295 Montpellier, France.ORCID 0000-0002-3498-3776
Inserm · FR

Funding

Agence Nationale pour le Développement de la Recherche en Santé ANR-11-INSB-005Association des Sclérodermiques de France NASociété Nationale Française de Médecine Interne NA
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a complex disorder resulting from dysregulated interactions between the three main pathophysiological axes: fibrosis, immune dysfunction, and vasculopathy, with no specific treatment available to date. Adipose tissue-derived mesenchymal stromal cells (ASCs) and their extracellular vesicles (EVs) have proved efficacy in pre-clinical murine models of SSc. However, their precise action mechanism is still not fully understood. Because of the lack of availability of fibroblasts isolated from SSc patients (SSc-Fb), our aim was to determine whether a TGFβ1-induced model of human myofibroblasts (Tβ-Fb) could reproduce the characteristics of SSc-Fb and be used to evaluate the anti-fibrotic function of ASCs and their EVs. We found out that Tβ-Fb displayed the main morphological and molecular features of SSc-Fb, including the enlarged hypertrophic morphology and expression of several markers associated with the myofibroblastic phenotype. Using this model, we showed that ASCs were able to regulate the expression of most myofibroblastic markers on Tβ-Fb and SSc-Fb, but only when pre-stimulated with TGFβ1. Of interest, ASC-derived EVs were more effective than parental cells for improving the myofibroblastic phenotype. In conclusion, we provided evidence that Tβ-Fb are a relevant model to mimic the main characteristics of SSc fibroblasts and investigate the mechanism of action of ASCs. We further reported that ASC-EVs are more effective than parental cells suggesting that the TGFβ1-induced pro-fibrotic environment may alter the function of ASCs.

Indexed as

Adipose TissueAnimalsBiomarkersCell CommunicationDisease SusceptibilityExtracellular VesiclesFibroblastsFibrosisHumansImmunophenotypingMesenchymal Stem CellsMiceMyofibroblastsScleroderma, SystemicTransforming Growth Factor beta1BiomarkersTransforming Growth Factor beta1anti-fibroticextracellular vesiclesmesenchymal stem cellssystemic sclerosisTGFβ1

Identifiers

PMID34202139
PMCPMC8269376
OpenAlexW3173569059

What Socratic 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 Socratic graph.