Evidence map›Paper›PMID 33761997›Full record

ArticleStem cell research & therapy2021

Exosomes from human umbilical cord mesenchymal stem cells attenuate the inflammation of severe steroid-resistant asthma by reshaping macrophage polarization.

Bing Dong, Chao Wang, Jing Zhang, Jinrong Zhang, Yinuo Gu, Xiaoping Guo, Xu Zuo, He Pan, Alan Chen-Yu Hsu, Guoqiang Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

82 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

22 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

11 authors at 2 institutions in 2 countries.

Bing DongDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Chao WangDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Jing ZhangDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Jinrong ZhangDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Yinuo GuDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Xiaoping GuoDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Xu ZuoDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
He PanDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Alan Chen-Yu HsuPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute and the University of Newcastle, Newcastle, NSW, 2305, Australia.
Guoqiang WangDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Fang WangDepartment of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China. wf@jlu.edu.cn.ORCID 0000-0003-0871-3454
Jilin University · CNHunter Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSevere, steroid-resistant asthma (SSRA) is a serious clinical problem in asthma management. Affected patients have severe clinical symptoms, worsened quality of life, and do not respond to steroid, a mainstay steroid treatment of asthma. Thus, effective therapies are urgently needed. Exosomes derived from mesenchymal stem cell (MSC-Exo) has become attractive candidates for the lung inflammatory diseases through its immunomodulatory effects. In this study, we explored the therapeutic effects of MSC-Exo in SSRA and identified the therapeutic mechanism of MSC-Exo.

methodExosomes from human umbilical cord mesenchymal stem cell (hUCMSC) were isolated and characterized by transmission electron microscopy, nanoparticle tracking analysis and flow cytometry analysis. Effects of MSC-Exo on airway hyper responsiveness (AHR), inflammation, histopathology, and macrophage polarization in SSRA in mice were evaluated. Systematic depletion of macrophages determined the role of macrophages in the therapeutic effect of SSRA in mice. LPS-stimulated RAW 264.7 cell model was constructed to determine the underlying mechanism of MSC-Exo on macrophage polarization. qRT-PCR, Western blotting, immunofluorescence, and flow cytometry were performed to evaluate the expression of M1 or M2 markers. Tandem mass tags (TMT)-labeled quantitative proteomics were applied to explore the central protein during the regulation effect of MSC-Exo on macrophage polarization. Knockdown and overexpression of TRAF1 were used to further clarify the role of the central protein on macrophage polarization.

resultWe successfully isolated and characterized exosomes from hUCMSCs. We verified that the intratracheal administration of MSC-Exo reversed AHR, histopathology changes, and inflammation in SSRA mice. Systematic depletion of macrophages weakened the therapeutic effect of MSC-Exo. We found that MSC-Exo treatment inhibited M1 polarization and promoted M2 polarization in LPS-stimulated RAW 264.7 cells. Subsequently, tumor necrosis factor receptor-associated factor 1 (TRAF1) was determined as the central protein which may be closely related to the regulation of macrophage polarization from TMT-labeled quantitative proteomics analysis. Knockdown and overexpression of TRAF1 demonstrated that the effect of MSC-Exo treatment on macrophage polarization, NF-κB and PI3K/AKT signaling was dependent on TRAF1.

conclusionMSC-Exo can ameliorate SSRA by moderating inflammation, which is achieved by reshaping macrophage polarization via inhibition of TRAF1.

Indexed as

AsthmaExosomesMesenchymal Stem CellsAnimalsHumansInflammationMacrophagesMicePhosphatidylinositol 3-KinasesQuality of LifeSteroidsUmbilical CordPhosphatidylinositol 3-KinasesSteroidsExosomeInflammationMacrophage polarizationMesenchymal stem cellSevere steroid-resistant asthma

Identifiers

PMID33761997
PMCPMC7988945
OpenAlexW3137097754

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.