Evidence map›Paper›PMID 25692676›Full record

ArticlePloS one2015

The notch signaling regulates CD105 expression, osteogenic differentiation and immunomodulation of human umbilical cord mesenchymal stem cells.

Tao Na, Jing Liu, Kehua Zhang, Min Ding, Bao-Zhu Yuan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Mesenchymal Stromal Cells as a Driver of Inflammaging.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
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  15. [Effects of tumor necrosis factor-α on osteogenic differentiation and Notch signaling pathway in human periodontal ligament stem cells].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2018
    Article
  16. Article
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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

5 authors at 2 institutions in 2 countries.

Tao NaCell Collection and Research Center, National Institutes for Food and Drug Control, Beijing, 100050, China.
Jing LiuCell Collection and Research Center, National Institutes for Food and Drug Control, Beijing, 100050, China.
Kehua ZhangCell Collection and Research Center, National Institutes for Food and Drug Control, Beijing, 100050, China.
Min DingNational Institute for Occupational Safety and Health, Morgantown, West Virginia, 26505, United States of America.
Bao-Zhu YuanCell Collection and Research Center, National Institutes for Food and Drug Control, Beijing, 100050, China.
National Institutes for Food and Drug Control · CNNational Institute for Occupational Safety and Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are a group of multipotent cells with key properties of multi-lineage differentiation, expressing a set of relatively specific surface markers and unique immunomodulatory functions. IDO1, a catabolic enzyme of tryptophan, represents a critical molecule mediating immunomodulatory functions of MSCs. However, the signaling pathways involved in regulating these key properties still remain elusive. To investigate the involvement of Notch signaling as well as other potential signaling pathway(s) in regulating these critical properties of MSCs, we treated human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) with γ-secreatase inhibitor I (GSI-I), which inhibits both Notch signaling and ubiquitin-proteasome activities. It was shown that the GSI-I treatment resulted in apoptosis, reduced expression of surface markers CD73, CD90 and CD105, reduced osteogenic differentiation, and reduction of the hUC-MSCs-mediated suppression of Th1 lymphocyte proliferation and the IFN-γ-induced IDO1 expression. Through distinguishing the effects of GSI-I between Notch inhibition and proteasome inhibition, it was further observed that, whereas both Notch inhibition and proteasome inhibition were attributable to the reduced CD105 expression and osteogenic differentiation, but not to the induced apoptosis. However, Notch inhibition, but not proteasome inhibition, only contributed to the significant effect of GSI-I on Th1 proliferation probably through reducing IDO1 promoter activity. In conclusion, the Notch signaling may represent a very important cell signaling capable of regulating multiple critical properties, especially the immunomodulatory functions of MSCs.

Indexed as

Antigens, CDCell DifferentiationCell ProliferationCells, CulturedCoculture TechniquesEndoglinGene Expression RegulationHumansImmunomodulationIndoleamine-Pyrrole 2,3,-DioxygenaseMesenchymal Stem CellsOligopeptidesOsteogenesisReceptors, Cell SurfaceReceptors, NotchSignal TransductionAntigens, CDbenzyloxycarbonyl-leucyl-leucyl-norleucinalEndoglinENG protein, humanIDO1 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseOligopeptidesReceptors, Cell SurfaceReceptors, Notch

Identifiers

PMID25692676
PMCPMC4334899
OpenAlexW2079977815

What OpenQuestion holds

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LicenceCC0
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.