Evidence map›Paper›PMID 24690886›Full record

ArticlePloS one2014

Pathogen sensing pathways in human embryonic stem cell derived-endothelial cells: role of NOD1 receptors.

Daniel M Reed, Gabor Foldes, Timothy Gatheral, Koralia E Paschalaki, Zsuzsanna Lendvai, Zsolt Bagyura, Tamas Nemeth, Judit Skopal, Bela Merkely, Aurica G Telcian and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Trial
  2. Article
  3. Review
  4. Innate immunity in stem cell-derived hepatocytes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  5. Article
  6. Article
  7. 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

17 authors at 4 institutions in 3 countries.

Daniel M ReedDepartment of Cardiothoracic Pharmacology, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Gabor FoldesDepartment of Cardiac Pharmacology, National Heart and Lung Institute, Imperial Centre for Translational and Experimental Medicine, Imperial College London, London, United Kingdom; Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Timothy GatheralDepartment of Cardiothoracic Pharmacology, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Koralia E PaschalakiAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Zsuzsanna LendvaiHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Zsolt BagyuraHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Tamas NemethHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Judit SkopalHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Bela MerkelyHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Aurica G TelcianMRC and Asthma UK Centre in Allergic Mechanisms of Asthma and Centre for Respiratory Infection, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Leila GogsadzeMRC and Asthma UK Centre in Allergic Mechanisms of Asthma and Centre for Respiratory Infection, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Michael R EdwardsMRC and Asthma UK Centre in Allergic Mechanisms of Asthma and Centre for Respiratory Infection, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Peter J GoughPattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Philadelphia, Pennsylvania, United States of America.
John BertinPattern Recognition Receptor Discovery Performance Unit, Immuno-Inflammation Therapeutic Area, GlaxoSmithKline, Philadelphia, Pennsylvania, United States of America.
Sebastian L JohnstonMRC and Asthma UK Centre in Allergic Mechanisms of Asthma and Centre for Respiratory Infection, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Sian E HardingDepartment of Cardiac Pharmacology, National Heart and Lung Institute, Imperial Centre for Translational and Experimental Medicine, Imperial College London, London, United Kingdom.
Jane A MitchellDepartment of Cardiothoracic Pharmacology, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Imperial College London · GBSemmelweis University · HUAsthma UK · GBGlaxoSmithKline (United States) · US

Funding

British Heart Foundation FS/09/017/26810British Heart Foundation PG/09/078British Heart Foundation PG/09/078/27985British Heart Foundation RG/11/19/29264Medical Research Council G1000758Medical Research Council MR/L012618/1Wellcome TrustWellcome Trust 0852551Z108/Z
6 · The paper itself

Abstract

Human embryonic stem cell-derived endothelial cells (hESC-EC), as well as other stem cell derived endothelial cells, have a range of applications in cardiovascular research and disease treatment. Endothelial cells sense Gram-negative bacteria via the pattern recognition receptors (PRR) Toll-like receptor (TLR)-4 and nucleotide-binding oligomerisation domain-containing protein (NOD)-1. These pathways are important in terms of sensing infection, but TLR4 is also associated with vascular inflammation and atherosclerosis. Here, we have compared TLR4 and NOD1 responses in hESC-EC with those of endothelial cells derived from other stem cells and with human umbilical vein endothelial cells (HUVEC). HUVEC, endothelial cells derived from blood progenitors (blood outgrowth endothelial cells; BOEC), and from induced pluripotent stem cells all displayed both a TLR4 and NOD1 response. However, hESC-EC had no TLR4 function, but did have functional NOD1 receptors. In vivo conditioning in nude rats did not confer TLR4 expression in hESC-EC. Despite having no TLR4 function, hESC-EC sensed Gram-negative bacteria, a response that was found to be mediated by NOD1 and the associated RIP2 signalling pathways. Thus, hESC-EC are TLR4 deficient but respond to bacteria via NOD1. This data suggests that hESC-EC may be protected from unwanted TLR4-mediated vascular inflammation, thus offering a potential therapeutic advantage.

Indexed as

AnimalsEndothelial CellsGene Knockdown TechniquesHaemophilus InfectionsHaemophilus influenzaeHuman Embryonic Stem CellsHumansHuman Umbilical Vein Endothelial CellsInduced Pluripotent Stem CellsNod1 Signaling Adaptor ProteinRats, NudeReceptor-Interacting Protein Serine-Threonine Kinase 2RNA, Small InterferingStem Cell TransplantationToll-Like Receptor 4NOD1 protein, humanNod1 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2RIPK2 protein, humanRNA, Small InterferingTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID24690886
PMCPMC3972153
OpenAlexW2017224967

What OpenQuestion holds

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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.