Evidence map›Paper›PMID 24682451›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Conditioned media from mesenchymal stromal cells restore sodium transport and preserve epithelial permeability in an in vitro model of acute alveolar injury.

Arnaud Goolaerts, Nadia Pellan-Randrianarison, Jérôme Larghero, Valérie Vanneaux, Yurdagül Uzunhan, Thomas Gille, Nicolas Dard, Carole Planès, Michael A Matthay, Christine Clerici

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 178 citations in OpenAlex.

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  10. EVs vs. EVs: MSCs and Tregs as a source of invisible possibilities.Journal of molecular medicine (Berlin, Germany) · 2023
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17 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

10 authors at 5 institutions in 1 country.

Arnaud GoolaertsInstitut National de la Santé et de la Recherche Médicale, U773, Paris, France;
Nadia Pellan-RandrianarisonInstitut National de la Santé et de la Recherche Médicale, U773, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Unité Mixte de Recherche 773 and Unité Mixte de Recherche 940, Paris, France;
Jérôme LargheroUniversité Paris Diderot, Sorbonne Paris Cité, Unité Mixte de Recherche 773 and Unité Mixte de Recherche 940, Paris, France; AP-HP, Hôpital Saint Louis, Unité de Thérapie Cellulaire et CIC de Biothérapies, Paris, France; University Paris Diderot, Sorbonne Paris Cité, Paris, France;
Valérie VanneauxUniversité Paris Diderot, Sorbonne Paris Cité, Unité Mixte de Recherche 773 and Unité Mixte de Recherche 940, Paris, France; AP-HP, Hôpital Saint Louis, Unité de Thérapie Cellulaire et CIC de Biothérapies, Paris, France; University Paris Diderot, Sorbonne Paris Cité, Paris, France;
Yurdagül UzunhanUniversité Paris 13, Sorbonne Paris Cité, EA2363, Bobigny, France; AP-HP, Hôpital Avicenne, Bobigny, France; and.
Thomas GilleUniversité Paris 13, Sorbonne Paris Cité, EA2363, Bobigny, France; AP-HP, Hôpital Avicenne, Bobigny, France; and.
Nicolas DardUniversité Paris 13, Sorbonne Paris Cité, EA2363, Bobigny, France;
Carole PlanèsUniversité Paris 13, Sorbonne Paris Cité, EA2363, Bobigny, France; AP-HP, Hôpital Avicenne, Bobigny, France; and.
Michael A MatthayInstitut National de la Santé et de la Recherche Médicale, U773, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Unité Mixte de Recherche 773 and Unité Mixte de Recherche 940, Paris, France;
Christine ClericiInstitut National de la Santé et de la Recherche Médicale, U773, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Unité Mixte de Recherche 773 and Unité Mixte de Recherche 940, Paris, France; AP-HP, Hôpital Bichat, Paris, France christine.clerici@bch.aphp.fr.
Assistance Publique – Hôpitaux de Paris · FRDélégation Paris 7 · FRInserm · FRUniversité Paris Cité · FRHôpital Avicenne · FR

Funding

MECHANISMS OF ALVEOLAR EPITHELIAL FLUID CLEARANCER01HL051854 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 1994 to 2012
$4.4M
NHLBI NIH HHS HL-51854NHLBI NIH HHS R01 HL051854
6 · The paper itself

Abstract

Mesenchymal stromal cells (MSCs) or their media (MSC-M) were reported to reverse acute lung injury (ALI)-induced decrease of alveolar fluid clearance. To determine the mechanisms by which MSC-M exert their beneficial effects, an in vitro model of alveolar epithelial injury was created by exposing primary rat alveolar epithelial cells (AECs) to hypoxia (3% O2) plus cytomix, a combination of IL-1β, TNF-α, and IFN-γ. MSC-M were collected from human MSCs exposed for 12 h to either normoxia (MSC-M) or to hypoxia plus cytomix (HCYT-MSC-M). This latter condition was used to model the effect of alveolar inflammation and hypoxia on paracrine secretion of MSCs in the injured lung. Comparison of paracrine soluble factors in MSC media showed that the IL-1 receptor antagonist and prostaglandin E2 were markedly increased while keratinocyte growth factor (KGF) was twofold lower in HCYT-MSC-M compared with MSC-M. In AECs, hypoxia plus cytomix increased protein permeability, reduced amiloride-sensitive short-circuit current (AS-Isc), and also decreased the number of α-epithelial sodium channel (α-ENaC) subunits in the apical membrane. To test the effects of MSC media, MSC-M and HCYT-MSC-M were added for an additional 12 h to AECs exposed to hypoxia plus cytomix. MSC-M and HCYT-MSC-M completely restored epithelial permeability to normal. MSC-M, but not HCYT-MSC-M, significantly prevented the hypoxia plus cytomix-induced decrease of ENaC activity and restored apical α-ENaC channels. Interestingly, KGF-deprived MSC-M were unable to restore amiloride-sensitive sodium transport, indicating a possible role for KGF in the beneficial effect of MSC-M. These results indicate that MSC-M may be a preferable therapeutic option for ALI.

Indexed as

Alveolar Epithelial CellsAnimalsApoptosisBiological TransportCell HypoxiaCell Membrane PermeabilityCells, CulturedCulture Media, ConditionedDinoprostoneEpithelial Sodium ChannelsFibroblast Growth Factor 7HumansInflammation MediatorsInterleukin 1 Receptor Antagonist ProteinMaleMesenchymal Stem CellsCulture Media, ConditionedDinoprostoneEpithelial Sodium ChannelsFGF7 protein, humanFibroblast Growth Factor 7Inflammation MediatorsInterleukin 1 Receptor Antagonist ProteinSodiumgrowth factorshypoxiainflammationmembrane transportmesenchymal stem cellssodium channels

Identifiers

PMID24682451
PMCPMC4042188
OpenAlexW1989796399

What OpenQuestion 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 OpenQuestion graph.