Evidence map›Paper›PMID 12598328›Full record

ArticleThe American journal of pathology2003

Lack of platelet endothelial cell adhesion molecule-1 attenuates foreign body inflammation because of decreased angiogenesis.

Anna Solowiej, Purba Biswas, Donnasue Graesser, Joseph A Madri

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-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

37 citing papers in PubMed, 92 citations in OpenAlex.

  1. Prostaglandin EThe American journal of pathology · 2026
    Article
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  11. PECAM-1 isoforms, eNOS and endoglin axis in regulation of angiogenesis.Clinical science (London, England : 1979) · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Microvascular remodeling and wound healing: a role for pericytes.The international journal of biochemistry & cell biology · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. SHP-2 phosphatase activity is required for PECAM-1-dependent cell motility.American journal of physiology. Cell physiology · 2010
    Article
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

4 authors at 1 institution in 1 country.

Anna SolowiejDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Purba Biswas
Donnasue Graesser
Joseph A Madri
Yale University · US

Funding

PATHOLOGY OF ENDOTHELIAL NEOVASCULARIZATIONR37HL028373 · NHLBI · YALE UNIVERSITY · PI MADRI, JOSEPH A · 1999 to 2008
$4.6M
CHEMILUMINESCENCE IMMUNOASSAY FOR INSULINR43DK038797 · NIDDK · LONDON DIAGNOSTICS, INC. · PI HART, RUSSELL COLIN · 1987 to 1987
–
NHLBI NIH HHS R37 HL028373NHLBI NIH HHS R37-HL-28373NIDDK NIH HHS P0 1 DK 38797
6 · The paper itself

Abstract

Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a 130-kd member of the immunoglobulin superfamily of proteins, expressed on endothelial cells, leukocytes, and platelets. Antibody-blocking studies have implicated it in modulating leukocyte transmigration and angiogenesis. However, the generation of the PECAM-1 knockout mouse has shown that its function can be compensated for by similarly acting proteins because most acute inflammatory models proceed in a comparable manner in wild-type and knockout animals. We decided to examine the function of PECAM-1 in the chronic process of foreign body inflammation. We show that PECAM-1-deficient mice exhibit attenuated neutrophil infiltration in and around a subcutaneous polyvinyl acetyl implant. Bone marrow engraftment studies indicate that the lack of CD31 expression on the endothelium determines the diminished leukocyte accumulation in the knockout implants. Specifically, we find that decreased angiogenesis (as manifested by lower vessel density, decreased hemoglobin content, and less laminin deposition) correlates with lower neutrophil accumulation in the knockout animals. This study indicates that the absence of endothelial PECAM-1 results in decreased angiogenesis and therefore in diminished delivery of leukocytes to the foreign body implants.

Indexed as

AnimalsBone Marrow TransplantationEndothelium, VascularForeign BodiesHemoglobinsInflammationLeukocytesMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicNeutrophilsPeroxidasePlatelet Endothelial Cell Adhesion Molecule-1PolyvinylsProstheses and ImplantsHemoglobinsPeroxidasePlatelet Endothelial Cell Adhesion Molecule-1polyvinyl acetatePolyvinyls

Identifiers

PMID12598328
PMCPMC1868115
OpenAlexW2020585843

What OpenQuestion holds

Textmetadata
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.