Evidence map›Paper›PMID 7878009›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Regulation of leukocyte-endothelium interaction and leukocyte transendothelial migration by intercellular adhesion molecule 1-fibrinogen recognition.

L R Languino, A Duperray, K J Joganic, M Fornaro, G B Thornton, D C Altieri

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

63 citing papers in PubMed, 189 citations in OpenAlex.

  1. Review
  2. Leukocyte kinetics and bacterial clearance duringAmerican journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  3. Article
  4. Review
  5. Fibrinogen and Factor XIII in Venous Thrombosis and Thrombus Stability.Arteriosclerosis, thrombosis, and vascular biology · 2022
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Injectable scaffolds: Preparation and application in dental and craniofacial regeneration.Materials science & engineering. R, Reports : a review journal · 2017
    Article
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

L R LanguinoDepartment of Vascular Biology, Scripps Research Institute, La Jolla, CA 92037.
A Duperray
K J Joganic
M Fornaro
G B Thornton
D C Altieri
Scripps Research Institute · US

Funding

Molecular Pathology of Vascular InjuryR37HL054131 · NHLBI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2004 to 2013
$3.1M
MOLECULAR PATHOLOGY OF VASCULAR INJURYR01HL054131 · NHLBI · YALE UNIVERSITY · PI ALTIERI, DARIO C. · 1994 to 2003
$1.0M
MAC 1 DEPENDENT REGULATION OF COAGULATIONR01HL043773 · NHLBI · YALE UNIVERSITY · PI ALTIERI, DARIO C. · 1990 to 1999
–
NHLBI NIH HHS HL-54131NHLBI NIH HHS R01 HL-43773
6 · The paper itself

Abstract

Although primarily recognized for its role in hemostasis, fibrinogen is also required for competent inflammatory reactions in vivo. It is now shown that fibrinogen promotes adhesion to and migration across an endothelial monolayer of terminally differentiated myelomonocytic cells. This process does not require chemotactic/haptotactic gradients or cytokine stimulation of the endothelium and is specific for the association of fibrinogen with intercellular adhesion molecule 1 (ICAM-1) on endothelium. Among other adhesive plasma proteins, fibronectin fails to increase the binding of leukocytes to endothelium, or transendothelial migration, whereas vitronectin promotes the binding but not the migration. The fibrinogen-mediated leukocyte adhesion and transendothelial migration could be inhibited by a peptide from the fibrinogen gamma-chain sequence N117NQKIVNL-KEKVAQLEA133, which blocks the binding of fibrinogen to ICAM-1. This interaction could also be inhibited by new anti-ICAM-1 monoclonal antibodies that did not affect the ICAM-1-CD11a/CD18 recognition, thus suggesting that the fibrinogen binding site on ICAM-1 may be structurally distinct from regions previously implicated in leukocyte-endothelium interaction. Therefore, binding of fibrinogen to vascular cell receptors is sufficient to initiate (i) increased leukocyte adhesion to endothelium and (ii) leukocyte transendothelial migration. These two processes are the earliest events of immune inflammatory responses and may also contribute to atherosclerosis.

Indexed as

Amino Acid SequenceAntibodies, MonoclonalBinding SitesCell AdhesionCell MovementEndothelium, VascularFibrinogenHumansIntercellular Adhesion Molecule-1In Vitro TechniquesLeukocytesMolecular Sequence DataPeptidesAntibodies, MonoclonalFibrinogenIntercellular Adhesion Molecule-1Peptides

Identifiers

PMID7878009
PMCPMC42548
OpenAlexW1980576110

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.