Evidence map›Paper›PMID 8691131›Full record

ArticleThe Journal of experimental medicine1996

Activation and homologous desensitization of human endothelial cells by CD40 ligand, tumor necrosis factor, and interleukin 1.

K Karmann, W Min, W C Fanslow, J S Pober

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 115 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Platelets and cancer angiogenesis nexus.Cancer metastasis reviews · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Ferritin as a novel reporter gene for photoacoustic molecular imaging.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2012
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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.

K KarmannMolecular Cardiobiology Program, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA.
W Min
W C Fanslow
J S Pober
Yale University · US

Funding

Presentation of Alloantigen by Human Vascular CellsR01HL051014 · NHLBI · YALE UNIVERSITY · PI MANES, THOMAS DAVID, POBER, JORDAN S · 1994 to 2019
$10.4M
PROTEINS OF THE ENDOTHELIAL CELL SURFACER37HL036003 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S · 1992 to 2001
$664k
NHLBI NIH HHS R01 HL 51014NHLBI NIH HHS R37 HL 36003
6 · The paper itself

Abstract

We have reported previously that activation of human umbilical vein endothelial cells (HUVECs) through CD40, using a recombinant soluble form of trimerized CD40 ligand, leads to induction of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1). Here, we compare the effects of CD40 ligand with those of tumor necrosis factor (TNF) and interleukin 1 (IL-1). All three ligands induce transient increases in E-selectin (peak 4 h) and VCAM-1 (peak 8-24 h), as well as sustained increases in ICAM-1 (plateau 24 h). Quantitatively, TNF is more potent than IL-1, which is much more potent than CD40 ligand. The same hierarchy is observed for transcriptional activation of an E-selectin promoter reporter gene construct in transiently transfected HUVECs. TNF and CD40 ligand each induced activation of the transcription factors NF-kappa B, IRF-1, and ATF-2/c-Jun, measured by electrophoretic mobility shift assays, but this response appeared quantitatively similar. All three agents transiently (peak 30 min) activated Jun NH2-terminal kinase (JNK), which has been implicated in transcription of E-selectin through its actions on ATF-2/c-Jun. Activation of JNK again showed a hierarchy of potency (TNF > IL-1 >> CD40 ligand), although the time course of induction was similar for all three agents. After 44 h of pretreatment, TNF, IL-1, and CD40 ligand each display homologous desensitization for reinduction of surface expression of E-selectin. A similar pattern of homologous desensitization for reactivation of JNK was observed. We conclude that TNF, IL-1, and CD40 ligand all activate similar responses in ECs, and that homologous desensitization of JNK may explain the inability of individual cytokines to reinduce E-selectin expression.

Indexed as

Mitogen-Activated Protein KinasesBase SequenceCalcium-Calmodulin-Dependent Protein KinasesCD40 LigandCell Adhesion MoleculesEndothelium, VascularE-SelectinGene ExpressionHumansIntercellular Adhesion Molecule-1Interleukin-1JNK Mitogen-Activated Protein KinasesMembrane GlycoproteinsMolecular Sequence DataOligodeoxyribonucleotidesRNA, MessengerCalcium-Calmodulin-Dependent Protein KinasesCD40 LigandCell Adhesion MoleculesE-SelectinIntercellular Adhesion Molecule-1Interleukin-1JNK Mitogen-Activated Protein KinasesMembrane GlycoproteinsMitogen-Activated Protein KinasesOligodeoxyribonucleotidesRNA, MessengerTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID8691131
PMCPMC2192678
OpenAlexW2160229740

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.