Evidence map›Paper›PMID 16478887›Full record

ArticleBlood2006

Plasminogen inhibits TNFalpha-induced apoptosis in monocytes.

Jennifer W Mitchell, Nagyung Baik, Francis J Castellino, Lindsey A Miles

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. 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
1.3field-weighted citation impact, top 19% 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, 33 citations in OpenAlex.

  1. Article
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  12. New insights into the role of Plg-RKT in macrophage recruitment.International review of cell and molecular biology · 2014
    Review
  13. Plasminogen receptors: the first quarter century.Seminars in thrombosis and hemostasis · 2013
    Review
  14. The plasminogen receptor, Plg-R(KT), and macrophage function.Journal of biomedicine & biotechnology · 2012
    Review
  15. Cell surface remodeling by plasmin: a new function for an old enzyme.Journal of biomedicine & biotechnology · 2012
    Review
  16. Article
  17. Article
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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.

Jennifer W MitchellDepartment of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. jwmitch@scripps.edu
Nagyung Baik
Francis J Castellino
Lindsey A Miles
University of Notre Dame · US

Funding

STRUCTURE-FUNCTION STUDIES ON PLASMINOGEN AND PLASMINR01HL013423 · NHLBI · UNIVERSITY OF NOTRE DAME · PI CASTELLINO, FRANCIS J, LEE, SHAUN · 1985 to 2021
$7.9M
REGULATION OF THE PLASMINOGEN SYSTEMR01HL045934 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI MILES, LINDSEY A · 1990 to 2006
$2.5M
REGULATION OF FIBRINOLYSIS BY CELL SURFACESR01HL038272 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI MILES, LINDSEY A · 1994 to 2002
$961k
REGULATION OF FIBRINOLYSIS BY CELL SURFACESR29HL038272 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI MILES, LINDSEY A · 1988 to 1992
–
STRUCTURE/FUNCTION STUDIES ON PLASMINOGEN AND PLASMINR37HL013423 · NHLBI · UNIVERSITY OF NOTRE DAME · PI CASTELLINO, FRANCIS J · 1990 to 1999
–
NHLBI NIH HHS HL07195NHLBI NIH HHS HL13423NHLBI NIH HHS HL38272NHLBI NIH HHS HL45934NIAID NIH HHS F32AI062042-01
6 · The paper itself

Abstract

Monocytes are major mediators of inflammation, and apoptosis provides a mechanism for regulating the inflammatory response by eliminating activated macrophages. Furthermore, as a consequence of apoptosis, plasminogen binding is markedly increased on monocytoid cells. Therefore, we investigated the ability of plasminogen to modulate monocyte apoptosis. Apoptosis of monocytoid cells (human monocytes and U937 cells) was induced with either TNFalpha or cycloheximide. When apoptosis was induced in the presence of increasing concentrations of plasminogen, apoptosis was inhibited in a dose-dependent manner with full inhibition achieved at 2 microM plasminogen. Plasminogen treatment also markedly reduced internucleosomal DNA fragmentation and reduced levels of active caspase 3, caspase 8, and caspase 9 induced by TNFalpha or by cycloheximide. We examined the requirement for plasmin proteolytic activity in the cytoprotective function of plasminogen. A plasminogen active site mutant, [D(646)E]-Plg, failed to recapitulate the cytoprotective effect of wild-type plasminogen. Furthermore, antibodies against PAR1 blocked the antiapoptotic effect of plasminogen. Our results suggest that plasminogen inhibits monocyte apoptosis. The cytoprotective effect of plasminogen requires plasmin proteolytic activity and requires PAR1. Because apoptosis of monocytes plays a key role in inflammation and atherosclerosis, these results provide insight into a novel role of plasminogen in these processes.

Indexed as

Amino Acid SubstitutionApoptosisCaspasesCells, CulturedDNA FragmentationDose-Response Relationship, DrugFibrinolysinHumansMonocytesPlasminogenReceptor, PAR-1Tumor Necrosis Factor-alphaCaspasesFibrinolysinPlasminogenReceptor, PAR-1Tumor Necrosis Factor-alpha

Identifiers

PMID16478887
PMCPMC1895791
OpenAlexW1993663536

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.