Evidence map›Paper›PMID 19189342›Full record

ArticleJournal of cellular physiology2009

Concentration dependent dual effect of thrombin in endothelial cells via Par-1 and Pi3 Kinase.

Jong-Sup Bae, Yong-Ung Kim, Moon-Ki Park, Alireza R Rezaie

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-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

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  8. Review
  9. Intracellular communication and immunothrombosis in sepsis.Journal of thrombosis and haemostasis : JTH · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Signaling pathways and intervention therapies in sepsis.Signal transduction and targeted therapy · 2021
    Review
  14. Review
  15. Thrombomodulin is essential for maintaining quiescence in vascular endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 2 countries.

Jong-Sup BaeDepartment of Herbal Pharmaceutical Engineering, College of Herbal Bio-Industry, Daegu Haany University, Gyeongsan, Republic of Korea. BaeJS@dhu.ac.kr
Yong-Ung Kim
Moon-Ki Park
Alireza R Rezaie
Daegu Haany University · KRSaint Louis University · US

Funding

Serpin Regulation of Coagulation ProteasesR01HL062565 · NHLBI · SAINT LOUIS UNIVERSITY · PI REZAIE, ALIREZA R. · 1999 to 2020
$6.2M
Molecular Basis of Coagulation Protease SpecificityR01HL068571 · NHLBI · SAINT LOUIS UNIVERSITY · PI REZAIE, ALIREZA R. · 2002 to 2010
$3.1M
NHLBI NIH HHS HL 62565NHLBI NIH HHS HL 68571NHLBI NIH HHS R01 HL062565NHLBI NIH HHS R01 HL068571
6 · The paper itself

Abstract

Disruption of endothelial barrier is a critical pathophysiological factor in inflammation. Thrombin exerts a variety of cellular effects including inflammation and apoptosis through activation of the protease activated receptors (PARs). The activation of PAR-1 by thrombin is known to have a bimodal effect in endothelial cell permeability with a low concentration (pM levels) eliciting a barrier protective and a high concentration (nM levels) eliciting a barrier disruptive response. It is not known whether this PAR-1-dependent activity of thrombin is a unique phenomenon specific for the in vitro assay or it is part of a general anti-inflammatory effect of low concentrations of thrombin that may have a physiological relevance. Here, we report that low concentrations of thrombin or of PAR-1 agonist peptide induced significant anti-inflammatory activities. However, relatively high concentration of thrombin or of PAR-1 agonist peptide showed pro-inflammatory activities. By using function-blocking anti-PAR-1 antibodies and PI3 kinase inhibitor, we show that the direct anti-inflammatory effects of low concentrations of thrombin are dependent on the activation of PAR-1 and PI3 kinase. These results suggest a role for cross communication between PAR-1 activation and PI3 kinase pathway in mediating the cytoprotective effects of low concentrations of thrombin in the cytokine-stimulated endothelial cells. J. Cell. Physiol. 219: 744-751, 2009. (c) 2009 Wiley-Liss, Inc.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalCell AdhesionCell Adhesion MoleculesCell Membrane PermeabilityCells, CulturedDose-Response Relationship, DrugEndothelial CellsHumansIn Vitro TechniquesNeutrophilsOligopeptidesPhosphatidylinositol 3-KinasesReceptor, PAR-1ThrombinTumor Necrosis Factor-alphaAnti-Inflammatory Agents, Non-SteroidalCell Adhesion MoleculesOligopeptidesPhosphatidylinositol 3-KinasesReceptor, PAR-1threonyl-phenylalanyl-leucyl-leucyl-arginyl-asparagineThrombinTumor Necrosis Factor-alpha

Identifiers

PMID19189342
PMCPMC2663600
OpenAlexW1970339861

What OpenQuestion holds

Textmetadata
LicenceTDM
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.