Evidence map›Paper›PMID 26898191›Full record

ArticleLeukemia2016

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1.

L Zanotti, R Angioni, B Calì, C Soldani, C Ploia, F Moalli, M Gargesha, G D'Amico, S Elliman, G Tedeschi and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.4field-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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  18. CD73Journal of extracellular vesicles · 2020
    Article
  19. Article
  20. Mesenchymal stem cells: From regeneration to cancer.Pharmacology & therapeutics · 2019
    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

16 authors at 10 institutions in 5 countries.

L ZanottiHumanitas Clinical and Research Institute, IRCCS, Rozzano, Milan, Italy.
R AngioniDepartment of Biomedical Sciences, Venetian Institute of Molecular Medicine (VIMM), Padua, Italy.
B CalìDepartment of Biomedical Sciences, Venetian Institute of Molecular Medicine (VIMM), Padua, Italy.
C SoldaniHumanitas Clinical and Research Institute, IRCCS, Rozzano, Milan, Italy.
C PloiaHumanitas Clinical and Research Institute, IRCCS, Rozzano, Milan, Italy.
F MoalliTheodor Kocher Institute, University of Bern, Bern, Switzerland.
M GargeshaBioInVision Inc., Cleveland, OH, USA.
G D'AmicoCentro Ricerca 'M. Tettamanti,' Clinica Pediatrica Università degli Studi di Milano Bicocca, Monza, Italy.
S EllimanOrbsen Therapeutics Ltd, National University of Ireland, Galway, Ireland.
G TedeschiDepartment of Veterinary Science and Public Health, University of Milano, Milano, Italy.
E MaffioliFilarete Foundation, Milano, Italy.
A NegriDepartment of Veterinary Science and Public Health, University of Milano, Milano, Italy.
S ZacchignaInternational Centre for Genetic Engineering and Biotechnology (ICGEB), Padriciano, Trieste, Italy.
A SarukhanINSERM, Paris, France.
J V SteinTheodor Kocher Institute, University of Bern, Bern, Switzerland.
A ViolaDepartment of Biomedical Sciences, Venetian Institute of Molecular Medicine (VIMM), Padua, Italy.
Fondazione Filarete · ITHumanitas University · ITUniversity of Bern · CHUniversity of Padua · ITBioInVision (United States) · USInserm · FRInternational Centre for Genetic Engineering and Biotechnology · ITOllscoil na Gaillimhe – University of Galway · IEUniversity of Milano-Bicocca · ITVeneto Institute of Molecular Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSC) represent a promising therapeutic approach in many diseases in view of their potent immunomodulatory properties, which are only partially understood. Here, we show that the endothelium is a specific and key target of MSC during immunity and inflammation. In mice, MSC inhibit activation and proliferation of endothelial cells in remote inflamed lymph nodes (LNs), affect elongation and arborization of high endothelial venules (HEVs) and inhibit T-cell homing. The proteomic analysis of the MSC secretome identified the tissue inhibitor of metalloproteinase-1 (TIMP-1) as a potential effector molecule responsible for the anti-angiogenic properties of MSC. Both in vitro and in vivo, TIMP-1 activity is responsible for the anti-angiogenic effects of MSC, and increasing TIMP-1 concentrations delivered by an Adeno Associated Virus (AAV) vector recapitulates the effects of MSC transplantation on draining LNs. Thus, this study discovers a new and highly efficient general mechanism through which MSC tune down immunity and inflammation, identifies TIMP-1 as a novel biomarker of MSC-based therapy and opens the gate to new therapeutic approaches of inflammatory diseases.

Indexed as

Angiogenesis InhibitorsAnimalsEndothelial CellsGenetic VectorsGene Transfer TechniquesInflammationLymph NodesLymphocytesMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceTissue Inhibitor of Metalloproteinase-1Angiogenesis InhibitorsTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID26898191
PMCPMC4858586
OpenAlexW2291917453

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.