Evidence map›Paper›PMID 36209115›Full record

ArticleStem cell research & therapy2022

New mechanism for mesenchymal stem cell microvesicle to restore lung permeability: intracellular S1P signaling pathway independent of S1P receptor-1.

Lifang Ye, Jieqiong Song, Yijun Zheng, Ming Zhong, Jun Liu, Duming Zhu, Shuling Hu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Frontiers in microbiology · 2023
    Article
  6. Review
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 3 institutions in 1 country.

Lifang YeDepartment of Intensive Care Medicine, Medical School, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, China.
Jieqiong SongDepartment of Intensive Care Medicine, Medical School, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, China.
Yijun ZhengDepartment of Intensive Care Medicine, Medical School, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, China.
Ming ZhongDepartment of Intensive Care Medicine, Medical School, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, China.
Jun LiuDepartment of Intensive Care Medicine, Gusu School, Suzhou Hospital, Nanjing Medical University, No 16 West Baita Road, Suzhou, 215001, China.
Duming Zhu *Department of Intensive Care Medicine, Medical School, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, China. duming_zhu@163.com.
Shuling Hu *Department of Intensive Care Medicine, Medical School, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Xuhui District, Shanghai, 200032, China. shulinghu2013@163.com.ORCID 0000-0002-7301-4564
Sun Yat-sen University · CNFudan University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicrovesicles (MVs) derived from human bone marrow mesenchymal stem cell (MSC) were demonstrated to restore lung protein permeability and attenuate acute lung injury. In our previous study, we found that MSC MV increased sphingosine-1-phosphate (S1P) kinase1 mRNA levels in injured human lung microvascular endothelial cells (HLMVEC) significantly. However, the role of S1P signaling in MSC MV to restore lung protein permeability is unknown.

methodsIn this study, we hypothesized that MSC MV might restore lung permeability in part through increasing intracellular S1P signaling pathway in injured HLMVEC independent of S1P receptors. We used the transwell co-culture system to study the effect of MSC MV on protein permeability of Lipopolysaccharide (LPS) damaged HLMVEC.

resultsOur results showed that LPS significantly increased the permeability of HLMVEC to FITC-dextran (70 kDa) within 24 h. MSC MV restores this permeability and, to a large extent, prevents the cytoskeleton protein F-actin from recombining into "actin stress fibers," and restores the positions of tight junctions and adhesion junctions in the damaged HLMVEC. This therapeutic effect of MSC MV was related to the increase in the S1P level in injured HLMVEC and was not eliminated when adding the antagonist of S1P receptor, suggesting that MSC MV to restore lung permeability was independent of S1P receptors on HLMVEC. Laser confocal further observed that Ca

conclusionsIn short, MSC MV partially restored protein permeability across HLMVEC through the intracellular S1P signaling pathway independent of S1P receptor-1.

Indexed as

LipopolysaccharidesMesenchymal Stem CellsActinsCapillary PermeabilityEndothelial CellsHumansLungLysophospholipidsPermeabilityRNA, MessengerSignal TransductionSphingosineSphingosine-1-Phosphate ReceptorsActinsLipopolysaccharidesLysophospholipidsRNA, MessengerS1PR1 protein, humanSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate ReceptorsHuman lung microvascular endothelial cellMesenchymal stem cellMicrovesiclesPulmonary endothelial permeabilitySphingosine-1-phosphate

Identifiers

PMID36209115
PMCPMC9548125
OpenAlexW4303650461

What OpenQuestion holds

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LicenceCC BY
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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.