Evidence map›Paper›PMID 27409608›Full record

ArticleInternational journal of molecular sciences2016

Identification of Pathways in Liver Repair Potentially Targeted by Secretory Proteins from Human Mesenchymal Stem Cells.

Sandra Winkler, Madlen Hempel, Sandra Brückner, Hans-Michael Tautenhahn, Roland Kaufmann, Bruno Christ

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Sandra WinklerApplied Molecular Hepatology Laboratory, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany. sandra.pelz@medizin.uni-leipzig.de.
Madlen HempelApplied Molecular Hepatology Laboratory, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany. madlen.hempel@medizin.uni-leipzig.de.
Sandra BrücknerApplied Molecular Hepatology Laboratory, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany. sandra.brueckner@medizin.uni-leipzig.de.
Hans-Michael TautenhahnApplied Molecular Hepatology Laboratory, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany. hans-michael.tautenhahn@medizin.uni-leipzig.de.
Roland KaufmannDepartment of General, Visceral and Vascular Surgery, Jena University Hospital, Erlanger Allee 101, 07747 Jena, Germany. roland.kaufmann@med.uni-jena.de.
Bruno ChristApplied Molecular Hepatology Laboratory, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany. bruno.christ@medizin.uni-leipzig.de.
University Hospital Leipzig · DEJena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe beneficial impact of mesenchymal stem cells (MSC) on both acute and chronic liver diseases has been confirmed, although the molecular mechanisms behind it remain elusive. We aim to identify factors secreted by undifferentiated and hepatocytic differentiated MSC in vitro in order to delineate liver repair pathways potentially targeted by MSC.

methodsSecreted factors were determined by protein arrays and related pathways identified by biomathematical analyses.

resultsMSC from adipose tissue and bone marrow expressed a similar pattern of surface markers. After hepatocytic differentiation, CD54 (intercellular adhesion molecule 1, ICAM-1) increased and CD166 (activated leukocyte cell adhesion molecule, ALCAM) decreased. MSC secreted different factors before and after differentiation. These comprised cytokines involved in innate immunity and growth factors regulating liver regeneration. Pathway analysis revealed cytokine-cytokine receptor interactions, chemokine signalling pathways, the complement and coagulation cascades as well as the Januskinase-signal transducers and activators of transcription (JAK-STAT) and nucleotide-binding oligomerization domain-like receptor (NOD-like receptor) signalling pathways as relevant networks. Relationships to transforming growth factor β (TGF-β) and hypoxia-inducible factor 1-α (HIF1-α) signalling seemed also relevant.

conclusionMSC secreted proteins, which differed depending on cell source and degree of differentiation. The factors might address inflammatory and growth factor pathways as well as chemo-attraction and innate immunity. Since these are prone to dysregulation in most liver diseases, MSC release hepatotropic factors, potentially supporting liver regeneration.

Indexed as

Activated-Leukocyte Cell Adhesion MoleculeAdipose TissueBone Marrow CellsCell DifferentiationCells, CulturedChemokinesCytokinesHumansHypoxia-Inducible Factor 1, alpha SubunitIntercellular Adhesion Molecule-1LiverLiver RegenerationMesenchymal Stem CellsNLR ProteinsPhenotypeSignal TransductionActivated-Leukocyte Cell Adhesion MoleculeChemokinesCytokinesHypoxia-Inducible Factor 1, alpha SubunitIntercellular Adhesion Molecule-1NLR ProteinsTransforming Growth Factor betaadipose tissuebone marrowchemokinescytokineshepatocytic differentiationliver regenerationmesenchymal stem cellssecretome

Identifiers

PMID27409608
PMCPMC4964475
OpenAlexW2466754089

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.