Evidence map›Paper›PMID 37153544›Full record

ArticleFrontiers in immunology2023

Endothelial ACKR1 is induced by neutrophil contact and down-regulated by secretion in extracellular vesicles.

Xinying Guo, Negar Khosraviani, Sneha Raju, Joshya Singh, Nikki Zamani Farahani, Madlene Abramian, Victor J Torres, Kathryn L Howe, Jason E Fish, Andras Kapus and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

14 citing papers in PubMed, 47 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 5 institutions in 2 countries.

Xinying GuoKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
Negar KhosravianiKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
Sneha RajuToronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.
Joshya SinghKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
Nikki Zamani FarahaniKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
Madlene AbramianKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
Victor J TorresDepartment of Microbiology, New York University Grossman School of Medicine, New York, NY, United States.
Kathryn L HoweToronto General Hospital Research Institute, University Health Network, Toronto, ON, Canada.
Jason E FishDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Andras KapusKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
Warren L LeeKeenan Centre for Biomedical Research, St. Michael's Hospital, Toronto, ON, Canada.
St. Michael's Hospital · CAToronto General Hospital · CAUniversity of Toronto · CANew York University · USUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atypical chemokine receptor-1 (ACKR1), previously known as the Duffy antigen receptor for chemokines, is a widely conserved cell surface protein that is expressed on erythrocytes and the endothelium of post-capillary venules. In addition to being the receptor for the parasite causing malaria, ACKR1 has been postulated to regulate innate immunity by displaying and trafficking chemokines. Intriguingly, a common mutation in its promoter leads to loss of the erythrocyte protein but leaves endothelial expression unaffected. Study of endothelial ACKR1 has been limited by the rapid down-regulation of both transcript and protein when endothelial cells are extracted and cultured from tissue. Thus, to date the study of endothelial ACKR1 has been limited to heterologous over-expression models or the use of transgenic mice. Here we report that exposure to whole blood induces ACKR1 mRNA and protein expression in cultured primary human lung microvascular endothelial cells. We found that contact with neutrophils is required for this effect. We show that NF-κB regulates ACKR1 expression and that upon removal of blood, the protein is rapidly secreted by extracellular vesicles. Finally, we confirm that endogenous ACKR1 does not signal upon stimulation with IL-8 or CXCL1. Our observations define a simple method for inducing endogenous endothelial ACKR1 protein that will facilitate further functional studies.

Indexed as

Endothelial CellsExtracellular VesiclesAnimalsChemokinesDuffy Blood-Group SystemEndotheliumHumansMiceNeutrophilsReceptors, Cell SurfaceACKR1 protein, humanChemokinesDuffy Blood-Group SystemReceptors, Cell Surfaceatypical chemokine receptor 1Duffy antigenendotheliumextracellular vesiclesleukocidinneutrophil

Identifiers

PMID37153544
PMCPMC10160463
OpenAlexW4366774563

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.