Evidence map›Paper›PMID 19603257›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2009

Detection and characterization of soluble CD93 released during inflammation.

Mallary C Greenlee, Sarah A Sullivan, Suzanne Slater Bohlson

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
0.9field-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

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Immuno-PET Imaging of CD93 Expression withMolecular pharmaceutics · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. TheJournal of inflammation research · 2023
    Article
  10. Article
  11. CD93 in macrophages: A novel target for atherosclerotic plaque imaging?Journal of cellular and molecular medicine · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Radioimmunoimaging ofOncology letters · 2019
    Article
  18. Article
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

Mallary C GreenleeDepartment of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, IN 46556, USA. mgreenle@nd.edu
Sarah A Sullivan
Suzanne Slater Bohlson
University of Notre Dame · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD93 is a cell surface glycoprotein that is required for efficient engulfment of apoptotic cells via an unknown mechanism. Recently, it was demonstrated that CD93 is proteolytically cleaved from the surface of activated human monocytes and neutrophils in response to inflammatory signals in vitro and that a soluble form of CD93 (sCD93) exists in human plasma.

objectiveThe objective of this study was to examine the relationship among production of sCD93, inflammation, and engulfment of apoptotic cells.

methodsSterile peritonitis was induced in C57BL/6 mice, and lavage fluid was analyzed for presence of sCD93 by ELISA and Western blot. Cellular infiltrate was assessed by flow cytometry and analyzed for its capacity to shed CD93 in vitro. Peritoneal lavage fluid (PLF) was examined for its ability to regulate engulfment of apoptotic cells.

resultsThere was an 8.9-fold increase in sCD93 following induction of peritonitis. Macrophages accounted for the majority of infiltrating leukocytes into the peritoneum when sCD93 levels were highest. Inflammatory peritoneal macrophages constitutively shed CD93 in vitro suggesting that this cell type contributes to elevated levels of sCD93 in vivo. Inflammatory PLF from wild-type mice containing elevated sCD93 significantly enhanced engulfment of apoptotic cells in vitro when compared to inflammatory fluid from CD93-deficient mice.

conclusionsThese data demonstrate that inflammation triggers release of sCD93 in vivo, identify the inflammatory macrophage as a source of sCD93, and provide insight into the mechanism by which CD93 contributes to engulfment of apoptotic cells.

Indexed as

AnimalsApoptosisCell LineHumansInflammationMacrophagesMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutPeritonitisReceptors, Complementcomplement 1q receptorMembrane GlycoproteinsReceptors, Complement

Identifiers

PMID19603257
OpenAlexW2126575886

What OpenQuestion holds

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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.