Evidence map›Paper›PMID 11877318›Full record

ArticleBritish journal of pharmacology2002

Mechanisms of action of proteinase-activated receptor agonists on human platelets.

Ada W Y Chung, Paul Jurasz, Morley D Hollenberg, Marek W Radomski

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Molecular Mechanisms Linking Diabetes with Increased Risk of Thrombosis.International journal of molecular sciences · 2023
    Review
  6. Role of Prednisolone in Platelet Activation by Inhibiting TxAAnimals : an open access journal from MDPI · 2023
    Article
  7. Review
  8. Myricetin, the Main Flavonoid inFrontiers in pharmacology · 2019
    Article
  9. Review
  10. Review
  11. Temperature effects on the activity, shape, and storage of platelets from 13-lined ground squirrels.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2017
    Article
  12. Article
  13. Interaction between circulating cancer cells and platelets: clinical implication.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Platelets enhance neutrophil transendothelial migration via P-selectin glycoprotein ligand-1.American journal of physiology. Heart and circulatory physiology · 2011
    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 2 institutions in 1 country.

Ada W Y ChungDepartment of Pharmacology, University of Alberta, Edmonton, Alberta, T6G 2H7, Canada.
Paul Jurasz
Morley D Hollenberg
Marek W Radomski
University of Alberta · CAUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. We studied the activation of human platelets by thrombin and proteinase activated receptor (PAR)-activating peptides (PAR-APs) [SFLLRNPNDKYEPF-amide (TRAP), TFLLR-amide (PAR1AP) and AYPGKF-amide (PAR4AP)]. 2. PAR agonist-induced platelet aggregation, glycoprotein (GP) Ib and GPIIb/IIIa surface expression and ADP release were measured by light aggregometry, flow cytometry and chemiluminescence. 3. Aggregation inhibitors, including prostacyclin (PGI(2)), nitric oxide-releasing agent (S-nitroso-glutathione, GSNO), aspirin, apyrase, and phenanthroline were used to study the susceptibility of PAR agonist-induced aggregation to pharmacological inhibition. 4. Thrombin was the most potent platelet agonist, followed by PAR1AP, TRAP and PAR4AP. 5. The aggregatory potencies of PAR-APs were not modified by the aminopeptidase inhibitor, amastatin. 6. Subthreshold concentrations of PAR1AP potentiated the effects of PAR4AP to stimulate maximal aggregation. 7. Both PGI(2) and GSNO reduced PAR agonist-induced aggregation and diminished GPIIb/IIIa up-regulation. 8. PAR agonist-induced aggregation was aspirin-insensitive indicating a minor role for TXA(2). 9. In contrast, phenanthroline and apyrase significantly enhanced the anti-aggregatory effects of aspirin against thrombin-, PAR1AP- and TRAP-induced aggregation suggesting the involvement of ADP- and MMP-2-dependent pathways. 10. PAR4AP-induced aggregation (but not PAR1AP-induced aggregation) was entirely ADP-dependent (abolished by apyrase) and resistant to phenanthroline (MMP-2-independent). 11. Thus, the mechanisms of PAR1 and 4-induced platelet aggregation are distinct and depend differentially on their ability to interact with pathways of aggregation, along with the subsequent activation of GPIIb/IIIa receptors.

Indexed as

HumansIn Vitro TechniquesPeptidesPlatelet AggregationPlatelet Aggregation InhibitorsReceptor, PAR-1Receptor, PAR-2Receptors, ThrombinThrombinPeptidesPlatelet Aggregation Inhibitorsprotease-activated receptor 4Receptor, PAR-1Receptor, PAR-2Receptors, ThrombinThrombin

Identifiers

PMID11877318
PMCPMC1573223
OpenAlexW2070099006

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.