Evidence map›Paper›PMID 27352134›Full record

ArticlePloS one2016

CD34 Promotes Pathological Epi-Retinal Neovascularization in a Mouse Model of Oxygen-Induced Retinopathy.

Martin J Siemerink, Michael R Hughes, Marchien G Dallinga, Tomek Gora, Jessica Cait, Ilse M C Vogels, Bahar Yetin-Arik, Cornelis J F Van Noorden, Ingeborg Klaassen, Kelly M McNagny and 1 more

Erratum issuedAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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.

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  9. Endothelial-specific YY1 governs sprouting angiogenesis through directly interacting with RBPJ.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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  14. A Critical Analysis of the AvailableJournal of ophthalmology · 2017
    Review
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  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Martin J SiemerinkOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Michael R HughesDepartment of Medical Genetics, University of British Columbia, Vancouver, BC, Canada.ORCID http://orcid.org/0000-0002-7925-6070
Marchien G DallingaOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Tomek GoraOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Jessica CaitThe Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada.
Ilse M C VogelsOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Bahar Yetin-ArikOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Cornelis J F Van NoordenOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Ingeborg KlaassenOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.
Kelly M McNagnyDepartment of Medical Genetics, University of British Columbia, Vancouver, BC, Canada.
Reinier O SchlingemannOcular Angiogenesis Group, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sialomucins CD34 and podocalyxin (PODXL) are anti-adhesive molecules expressed at the luminal membrane of endothelial cells of small blood vessels and facilitate vascular lumen formation in the developing mouse aorta. CD34 transcript and protein levels are increased during human angiogenesis, its expression is particularly enriched on endothelial tip cell filopodia and CD34 is a marker for tip cells in vitro. Here, we investigated whether CD34 merely marks endothelial tip cells or has a functional role in tip cells and angiogenesis. We assessed that silencing CD34 in human microvascular endothelial cells has little effect on endothelial cell migration or invasion, but has a significant effect on vascular-endothelial growth factor-induced angiogenic sprouting activity in vitro. In vivo, the absence of CD34 reduced the density of filopodia on retinal endothelial tip cells in neonatal mice, but did not influence the overall architecture of the retinal vascular network. In oxygen-induced retinopathy, Cd34-/- mice showed normal intra-retinal regenerative angiogenesis but the number of pathological epi-retinal neovascular tufts were reduced. We conclude that CD34 is not essential for developmental vascularization in the retina, but its expression promotes the formation of pathological, invasive vessels during neovascularization.

Indexed as

AnimalsAntigens, CD34Cell LineCells, CulturedEndothelial CellsEndothelium, VascularHumansMiceMice, Inbred C57BLNeovascularization, PathologicOxygenRetinal VesselsRetinopathy of PrematuritySialoglycoproteinsAntigens, CD34OxygenpodocalyxinSialoglycoproteins

Identifiers

PMID27352134
PMCPMC4924789

What OpenQuestion holds

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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.