Evidence map›Paper›PMID 9916937›Full record

ArticleThe American journal of pathology1999

T lymphocytes induce endothelial cell matrix metalloproteinase expression by a CD40L-dependent mechanism: implications for tubule formation.

F Mach, U Schönbeck, R P Fabunmi, C Murphy, E Atkinson, J Y Bonnefoy, P Graber, P Libby

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 175 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Cardiovascular Effects Mediated by HMMR and CD44.Mediators of inflammation · 2021
    Review
  8. Observational
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. New frontiers for platelet CD154.Experimental hematology & oncology · 2015
    Article
  15. Review
  16. The role of hypoxia in orthodontic tooth movement.International journal of dentistry · 2013
    Review
  17. Review
  18. Matrix metalloproteinases in cytotoxic lymphocytes impact on tumour infiltration and immunomodulation.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2011
    Article
  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

8 authors at 2 institutions in 1 country.

F MachDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
U Schönbeck
R P Fabunmi
C Murphy
E Atkinson
J Y Bonnefoy
P Graber
P Libby
Brigham and Women's Hospital · USHarvard University · US

Funding

NUCLEAR FACTOR KAPPA BETA AND THE INITIATION OF THE ATHEROSCLEROTIC LESIONP50HL056985 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GIMBRONE, MICHAEL A · 1997 to 2006
$14.1M
NHLBI NIH HHS HL-56985NHLBI NIH HHS P50 HL056985
6 · The paper itself

Abstract

Neovascularization frequently accompanies chronic immune responses characterized by T cell infiltration and activation. Angiogenesis requires endothelial cells (ECs) to penetrate extracellular matrix, a process that involves matrix metalloproteinases (MMPs). We report here that activated human T cells mediate contact-dependent expression of MMPs in ECs through CD40/CD40 ligand signaling. Ligation of CD40 on ECs induced de novo expression of gelatinase B (MMP-9), increased interstitial collagenase (MMP-1) and stromelysin (MMP-3), and activated gelatinase A (MMP-2). Recombinant human CD40L induced expression of MMPs by human vascular ECs to a greater extent than did maximally effective concentrations of interleukin-1beta or tumor necrosis factor-alpha. Moreover, activation of human vascular ECs through CD40 induced tube formation in a three-dimensional fibrin matrix gel assay, an effect antagonized by a MMP inhibitor. These results demonstrated that activation of ECs by interaction with T cells induced synthesis and release of MMPs and promoted an angiogenic function of ECs via CD40L-CD40 signaling. As vascular cells at the sites of chronic inflammation, such as atherosclerotic plaques, express CD40 and its ligand, our findings suggest that ligation of CD40 on ECs can mediate aspects of vascular remodeling and neovessel formation during atherogenesis and other chronic immune reactions.

Indexed as

CapillariesCD40 AntigensCD40 LigandCells, CulturedCollagenasesEndothelium, VascularExtracellular MatrixGelatinasesHumansMatrix Metalloproteinase 3Membrane GlycoproteinsMetalloendopeptidasesRecombinant ProteinsTissue Inhibitor of Metalloproteinase-1T-LymphocytesCD40 AntigensCD40 LigandCollagenasesGelatinasesMatrix Metalloproteinase 3Membrane GlycoproteinsMetalloendopeptidasesRecombinant ProteinsTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID9916937
PMCPMC1853443
OpenAlexW1503875604

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.