Evidence map›Paper›PMID 36382783›Full record

ArticleEMBO reports2023

Endothelial transmigration hotspots limit vascular leakage through heterogeneous expression of ICAM-1.

Max L B Grönloh, Janine J G Arts, Sebastián Palacios Martínez, Amerens A van der Veen, Lanette Kempers, Abraham C I van Steen, Joris J T H Roelofs, Martijn A Nolte, Joachim Goedhart, Jaap D van Buul

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 44 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

10 authors at 3 institutions in 1 country.

Max L B Grönloh *Molecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.ORCID 0000-0003-0109-8225
Janine J G Arts *Molecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.
Sebastián Palacios MartínezMolecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.ORCID 0000-0001-6626-5798
Amerens A van der VeenMolecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.
Lanette KempersMolecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.
Abraham C I van SteenMolecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.ORCID 0000-0002-8023-352X
Joris J T H RoelofsDepartment of Pathology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Location AMC, Amsterdam, The Netherlands.ORCID 0000-0001-9595-6571
Martijn A NolteMolecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.ORCID 0000-0002-5447-0839
Joachim GoedhartSection Molecular Cytology at Swammerdam Institute for Life Sciences, Leeuwenhoek Centre for Advanced Microscopy, University of Amsterdam, Amsterdam, The Netherlands.ORCID 0000-0002-0630-3825
Jaap D van BuulMolecular Cell Biology Lab, Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands.ORCID 0000-0003-0054-7949
Sanquin · NLAmsterdam Neuroscience · NLUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon inflammation, leukocytes leave the circulation by crossing the endothelial monolayer at specific transmigration "hotspot" regions. Although these regions support leukocyte transmigration, their functionality is not clear. We found that endothelial hotspots function to limit vascular leakage during transmigration events. Using the photoconvertible probe mEos4b, we traced back and identified original endothelial transmigration hotspots. Using this method, we show that the heterogeneous distribution of ICAM-1 determines the location of the transmigration hotspot. Interestingly, the loss of ICAM-1 heterogeneity either by CRISPR/Cas9-induced knockout of ICAM-1 or equalizing the distribution of ICAM-1 in all endothelial cells results in the loss of TEM hotspots but not necessarily in reduced TEM events. Functionally, the loss of endothelial hotspots results in increased vascular leakage during TEM. Mechanistically, we demonstrate that the 3 extracellular Ig-like domains of ICAM-1 are crucial for hotspot recognition. However, the intracellular tail of ICAM-1 and the 4

Indexed as

Intercellular Adhesion Molecule-1Transendothelial and Transepithelial MigrationCell AdhesionCell MovementEndothelial CellsEndothelium, VascularLeukocytesSignal TransductionIntercellular Adhesion Molecule-1ICAM-1inflammationleakagetransendothelial migration hotspots

Identifiers

PMID36382783
PMCPMC9827561
OpenAlexW4309152025

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.