Evidence map›Paper›PMID 30279450›Full record

ArticleScientific reports2018

A systems-approach reveals human nestin is an endothelial-enriched, angiogenesis-independent intermediate filament protein.

Philip Dusart, Linn Fagerberg, Ljubica Perisic, Mete Civelek, Eike Struck, Ulf Hedin, Mathias Uhlén, David-Alexandre Trégouët, Thomas Renné, Jacob Odeberg and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 25 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

11 authors at 6 institutions in 4 countries.

Philip DusartScience for Life Laboratory, School of Biotechnology, Kungliga Tekniska Högskolan (KTH) Royal Institute of Technology, SE-171 21, Stockholm, Sweden.
Linn FagerbergScience for Life Laboratory, School of Biotechnology, Kungliga Tekniska Högskolan (KTH) Royal Institute of Technology, SE-171 21, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-0198-7137
Ljubica PerisicVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institute, SE-171 76, Stockholm, Sweden.
Mete CivelekDepartment of Biomedical Engineering, University of Virginia, Charlottesville, USA.ORCID http://orcid.org/0000-0002-8141-0284
Eike StruckScience for Life Laboratory, School of Biotechnology, Kungliga Tekniska Högskolan (KTH) Royal Institute of Technology, SE-171 21, Stockholm, Sweden.
Ulf HedinVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institute, SE-171 76, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-9212-3945
Mathias UhlénScience for Life Laboratory, School of Biotechnology, Kungliga Tekniska Högskolan (KTH) Royal Institute of Technology, SE-171 21, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4858-8056
David-Alexandre TrégouëtSorbonne Universités, UPMC Univ Paris 06, UMR_S 1166, Team Genomics & Pathophysiology of Cardiovascular Diseases, Paris, France.ORCID http://orcid.org/0000-0001-9084-7800
Thomas RennéInstitute for Clinical Chemistry and Laboratory Medicine, University Medical Centre Hamburg-Eppendorf, D-20246, Hamburg, Germany.
Jacob OdebergScience for Life Laboratory, School of Biotechnology, Kungliga Tekniska Högskolan (KTH) Royal Institute of Technology, SE-171 21, Stockholm, Sweden.
Lynn M ButlerScience for Life Laboratory, School of Biotechnology, Kungliga Tekniska Högskolan (KTH) Royal Institute of Technology, SE-171 21, Stockholm, Sweden. Lynn.Butler@ki.se.
Science for Life Laboratory · SEKarolinska Institutet · SEUniversität Hamburg · DEKarolinska University Hospital · SESorbonne Université · FRUniversity of Virginia · US

Funding

Stockholms Läns Landsting (Stockholm County Council) ALF2011-0260 and ALF-2011-0279Stockholms Läns Landsting (Stockholm County Council) LS 1302-0311Vetenskapsrådet (Swedish Research Council) 2013-42608-102305-28Vetenskapsrådet (Swedish Research Council) K2009-65X-2233-01-3, K2013-65X-06816-30-4 and 349-2007-8703
6 · The paper itself

Abstract

The intermediate filament protein nestin is expressed during embryonic development, but considered largely restricted to areas of regeneration in the adult. Here, we perform a body-wide transcriptome and protein-profiling analysis to reveal that nestin is constitutively, and highly-selectively, expressed in adult human endothelial cells (EC), independent of proliferative status. Correspondingly, we demonstrate that it is not a marker for tumour EC in multiple malignancy types. Imaging of EC from different vascular beds reveals nestin subcellular distribution is shear-modulated. siRNA inhibition of nestin increases EC proliferation, and nestin expression is reduced in atherosclerotic plaque neovessels. eQTL analysis reveals an association between SNPs linked to cardiovascular disease and reduced aortic EC nestin mRNA expression. Our study challenges the dogma that nestin is a marker of proliferation, and provides insight into its regulation and function in EC. Furthermore, our systems-based approach can be applied to investigate body-wide expression profiles of any candidate protein.

Indexed as

AdultAortaCardiovascular DiseasesCell MovementCell ProliferationCells, CulturedDatabases, GeneticDatasets as TopicEndothelial CellsEndothelium, VascularFemaleGene Expression ProfilingHaplotypesHumansMaleNeoplasmsNES protein, humanNestinRNA, Small Interfering

Identifiers

PMID30279450
PMCPMC6168570
OpenAlexW2893271207

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.