Evidence map›Paper›PMID 36961390›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2023

CD93 maintains endothelial barrier function by limiting the phosphorylation and turnover of VE-cadherin.

Roberta Lugano, Kalyani Vemuri, Stefano Barbera, Maurizio Orlandini, Elisabetta Dejana, Lena Claesson-Welsh, Anna Dimberg

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  13. UnravelingFrontiers in pharmacology · 2025
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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

7 authors at 2 institutions in 2 countries.

Roberta LuganoDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, 75185, Uppsala, Sweden.ORCID 0000-0002-7294-345X
Kalyani VemuriDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, 75185, Uppsala, Sweden.
Stefano BarberaDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, 75185, Uppsala, Sweden.
Maurizio OrlandiniDepartment of Biotechnology, Chemistry and Pharmacy, University of Siena, Via A. Moro, 2, 53100, Siena, Italy.
Elisabetta DejanaDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, 75185, Uppsala, Sweden.
Lena Claesson-WelshDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, 75185, Uppsala, Sweden.
Anna DimbergDepartment of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, 75185, Uppsala, Sweden.
Uppsala University · SEUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of vascular permeability to plasma is essential for tissue and organ homeostasis and is mediated by endothelial cell-to-cell junctions that tightly regulate the trafficking of molecules between blood and tissue. The single-pass transmembrane glycoprotein CD93 is upregulated in endothelial cells during angiogenesis and controls cytoskeletal dynamics. However, its role in maintaining homeostasis by regulating endothelial barrier function has not been elucidated yet. Here, we demonstrate that CD93 interacts with vascular endothelial (VE)-cadherin and limits its phosphorylation and turnover. CD93 deficiency in vitro and in vivo induces phosphorylation of VE-cadherin under basal conditions, displacing it from endothelial cell-cell contacts. Consistent with this, endothelial junctions are defective in CD93

Indexed as

CadherinsEndothelial CellsAdherens JunctionsAnimalsAntigens, CDCadherin 5Capillary PermeabilityCells, CulturedEndothelium, VascularMicePhosphorylationAntigens, CDCadherin 5Cadherinsblood-brain barrierCD93endothelial junctionsRhoGTPasesvascular permeabilityVE-cadherin

Identifiers

PMID36961390
PMCPMC11977521
OpenAlexW4360810365

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.