Evidence map›Paper›PMID 32098168›Full record

ArticleInternational journal of molecular sciences2020

Endothelial Semaphorin 3F Maintains Endothelial Barrier Function and Inhibits Monocyte Migration.

Huayu Zhang, Dianne Vreeken, Abidemi Junaid, Gangqi Wang, Wendy M P J Sol, Ruben G de Bruin, Anton Jan van Zonneveld, Janine M van Gils

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. New Promising Routes in Peptic Ulcers: Toll-like Receptors and Semaphorins.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
  3. Article
  4. Review
  5. 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

8 authors at 1 institution in 1 country.

Huayu ZhangEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Dianne VreekenEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Abidemi JunaidEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.ORCID 0000-0001-8562-7942
Gangqi WangEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Wendy M P J SolEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.ORCID 0000-0001-5913-436X
Ruben G de BruinEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Anton Jan van ZonneveldEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.ORCID 0000-0002-1676-7738
Janine M van GilsEinthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.ORCID 0000-0003-2429-7462
Leiden University Medical Center · NL

Funding

European Research Area Network on Cardiovascular Diseases 038 MISsCVDHartstichting 2013T127Hartstichting RECONNECT CVONZonMw MKMD 114022501
6 · The paper itself

Abstract

In normal physiology, endothelial cells (ECs) form a vital barrier between the blood and underlying tissue controlling leukocyte diapedesis and vascular inflammation. Emerging data suggest that neuronal guidance cues, typically expressed during development, have roles outside the nervous system in vascular biology and immune responses. In particular, Class III semaphorins have been reported to affect EC migration and angiogenesis. While ECs express high levels of semaphorin 3F (SEMA3F), little is known about its function in mature ECs. Here we show that SEMA3F expression is reduced by inflammatory stimuli and increased by laminar flow. Endothelial cells exposed to laminar flow secrete SEMA3F, which subsequently binds to heparan sulfates on the surface of ECs. However, under pro-inflammatory conditions, reduced levels of SEMA3F make ECs more prone to monocyte diapedesis and display impaired barrier function as measured with an electric cell-substrate impedance sensing system and a microfluidic system. In addition, we demonstrate that SEMA3F can directly inhibit the migration of activated monocytes. Taken together, our data suggest an important homeostatic function for EC-expressed SEMA3F, serving as a mediator of endothelial quiescence.

Indexed as

Transendothelial and Transepithelial MigrationEndothelium, VascularHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsInflammationMembrane ProteinsMonocytesNerve Tissue ProteinsMembrane ProteinsNerve Tissue ProteinsSEMA3F protein, humanendothelial cellsmonocytessemaphorin

Identifiers

PMID32098168
PMCPMC7073048
OpenAlexW3008360255

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.