Evidence map›Paper›PMID 38441970›Full record

ArticleJCI insight2024

CD93 maintains endothelial barrier function and limits metastatic dissemination.

Kalyani Vemuri, Beatriz de Alves Pereira, Patricia Fuenzalida, Yelin Subashi, Stefano Barbera, Luuk van Hooren, Marie Hedlund, Fredrik Pontén, Cecilia Lindskog, Anna-Karin Olsson and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 14 citations in OpenAlex.

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  19. Clinicopathological association of CD93 expression in gastric adenocarcinoma.Journal of cancer research and clinical oncology · 2024
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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

12 authors at 1 institution in 1 country.

Kalyani VemuriDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Beatriz de Alves PereiraDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Patricia FuenzalidaDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Yelin SubashiDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Stefano BarberaDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Luuk van HoorenDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Marie HedlundDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Fredrik PonténDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Cecilia LindskogDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Anna-Karin OlssonDepartment of Medical Biochemistry and Microbiology, Uppsala University Biomedical Center, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Roberta LuganoDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Anna DimbergDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, and.
Uppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Compromised vascular integrity facilitates extravasation of cancer cells and promotes metastatic dissemination. CD93 has emerged as a target for antiangiogenic therapy, but its importance for vascular integrity in metastatic cancers has not been evaluated. Here, we demonstrate that CD93 participates in maintaining the endothelial barrier and reducing metastatic dissemination. Primary melanoma growth was hampered in CD93-/- mice, but metastatic dissemination was increased and associated with disruption of adherens and tight junctions in tumor endothelial cells and elevated expression of matrix metalloprotease 9 at the metastatic site. CD93 directly interacted with vascular endothelial growth factor receptor 2 (VEGFR2) and its absence led to VEGF-induced hyperphosphorylation of VEGFR2 in endothelial cells. Antagonistic anti-VEGFR2 antibody therapy rescued endothelial barrier function and reduced the metastatic burden in CD93-/- mice to wild-type levels. These findings reveal a key role of CD93 in maintaining vascular integrity, which has implications for pathological angiogenesis and endothelial barrier function in metastatic cancer.

Indexed as

Endothelial CellsNeoplasmsAnimalsEndothelium, VascularMembrane GlycoproteinsMiceNeovascularization, PathologicReceptors, ComplementVascular Endothelial Growth Factor Acomplement 1q receptorMembrane GlycoproteinsReceptors, ComplementVascular Endothelial Growth Factor AEndothelial cellsExtracellular matrixMelanomaOncologyVascular biology

Identifiers

PMID38441970
PMCPMC11128212
OpenAlexW4392454415

What OpenQuestion holds

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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.