Evidence map›Paper›PMID 32787906›Full record

ArticleStem cell research & therapy2020

Reparative effect of mesenchymal stromal cells on endothelial cells after hypoxic and inflammatory injury.

Jesus M Sierra-Parraga, Ana Merino, Marco Eijken, Henri Leuvenink, Rutger Ploeg, Bjarne K Møller, Bente Jespersen, Carla C Baan, Martin J Hoogduijn

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.3field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 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

9 authors at 5 institutions in 3 countries.

Jesus M Sierra-ParragaInternal Medicine Department, Sector Nephrology & Transplantation, University Medical Center Rotterdam, Erasmus MC, Postbus 2040, 3000 CA, Rotterdam, the Netherlands. j.sierraparraga@erasmusmc.nl.ORCID 0000-0003-1062-3343
Ana MerinoInternal Medicine Department, Sector Nephrology & Transplantation, University Medical Center Rotterdam, Erasmus MC, Postbus 2040, 3000 CA, Rotterdam, the Netherlands.
Marco EijkenDepartment of Renal Medicine, Aarhus University Hospital, Aarhus, Denmark.
Henri LeuveninkDepartment of Surgery - Organ Donation and Transplantation, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Rutger PloegNuffield Department of Surgical Sciences and Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Bjarne K MøllerDepartment of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark.
Bente JespersenDepartment of Renal Medicine, Aarhus University Hospital, Aarhus, Denmark.
Carla C BaanInternal Medicine Department, Sector Nephrology & Transplantation, University Medical Center Rotterdam, Erasmus MC, Postbus 2040, 3000 CA, Rotterdam, the Netherlands.
Martin J HoogduijnInternal Medicine Department, Sector Nephrology & Transplantation, University Medical Center Rotterdam, Erasmus MC, Postbus 2040, 3000 CA, Rotterdam, the Netherlands.
Erasmus MC · NLAarhus University Hospital · DKAarhus University · DKUniversity Medical Center Groningen · NLUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe renal endothelium is a prime target for ischemia-reperfusion injury (IRI) during donation and transplantation procedures. Mesenchymal stromal cells (MSC) have been shown to ameliorate kidney function after IRI. However, whether this involves repair of the endothelium is not clear. Therefore, our objective is to study potential regenerative effects of MSC on injured endothelial cells and to identify the molecular mechanisms involved.

methodsHuman umbilical vein endothelial cells (HUVEC) were submitted to hypoxia and reoxygenation and TNF-α treatment. To determine whether physical interaction or soluble factors released by MSC were responsible for the potential regenerative effects of MSC on endothelial cells, dose-response experiments were performed in co-culture and transwell conditions and with secretome-deficient MSC.

resultsMSC showed increased migration and adhesion to injured HUVEC, mediated by CD29 and CD44 on the MSC membrane. MSC decreased membrane injury marker expression, oxidative stress levels, and monolayer permeability of injured HUVEC, which was observed only when allowing both physical and paracrine interaction between MSC and HUVEC. Furthermore, viable MSC in direct contact with injured HUVEC improved wound healing capacity by 45% and completely restored their angiogenic capacity. In addition, MSC exhibited an increased ability to migrate through an injured HUVEC monolayer compared to non-injured HUVEC in vitro.

conclusionsThese results show that MSC have regenerative effects on injured HUVEC via a mechanism which requires both physical and paracrine interaction. The identification of specific effector molecules involved in MSC-HUVEC interaction will allow targeted modification of MSC to apply and enhance the therapeutic effects of MSC in IRI.

Indexed as

Mesenchymal Stem CellsMesenchymal Stem Cell TransplantationReperfusion InjuryCoculture TechniquesHumansHuman Umbilical Vein Endothelial CellsHypoxiaAngiogenesisEndotheliumIschemia-reperfusion-injury (IRI)Mesenchymal stromal cells (MSC)Tissue repair

Identifiers

PMID32787906
PMCPMC7424997
OpenAlexW3048538050

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.