Evidence map›Paper›PMID 21652710›Full record

ArticleThe Journal of biological chemistry2011

The P2Y(2) nucleotide receptor mediates tissue factor expression in human coronary artery endothelial cells.

Ling Ding, Wanshu Ma, Timothy Littmann, Riley Camp, Jianzhong Shen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. The P2YThe Journal of biological chemistry · 2024
    Article
  4. Article
  5. P2YFrontiers in immunology · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Signaling Through Purinergic Receptor P2YInternational journal of molecular sciences · 2020
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. 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

5 authors at 1 institution in 1 country.

Ling DingDivision of Pharmacology, Department of Pharmacal Sciences, Harrison School of Pharmacy, Auburn University, Auburn, Alabama 36849, USA.
Wanshu Ma
Timothy Littmann
Riley Camp
Jianzhong Shen
Auburn University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery of the role of P2Y(12) receptor in platelet aggregation leads to a new anti-thrombotic drug Plavix; however, little is known about non-platelet P2Y receptors in thrombosis. This study tested the hypothesis that endothelial P2Y receptor(s) mediates up-regulation of tissue factor (TF), the initiator of coagulation cascade. Stimulation of human coronary artery endothelial cells (HCAEC) by UTP/ATP increased the mRNA level of TF but not of its counterpart-tissue factor pathway inhibitor, which was accompanied by up-regulation of TF protein and cell surface activity. RT-PCR revealed a selective expression of P2Y(2) and P2Y(11) receptors in HCAEC. Consistent with this, TF up-regulation was inhibited by suramin or by siRNA silencing of P2Y(2) receptor, but not by NF-157, a P2Y(11)-selective antagonist, suggesting a role for the P2Y(2) receptor. In addition, P2Y(2) receptor activated ERK1/2, JNK, and p38 MAPK pathways without affecting the positive NF-κB and negative AKT regulatory pathways of TF expression. Furthermore, TF up-regulation was abolished or partially suppressed by inhibition of p38 or JNK but not ERK1/2. Interestingly, blockade of the PLC/Ca(2+) pathway did not affect P2Y(2) receptor activation of p38, JNK, and TF induction. However, blockade of Src kinase reduced phosphorylation of p38 but not JNK, eliminating TF induction. In contrast, inhibition of Rho kinase reduced phosphorylation of JNK but not p38, decreasing TF expression. These findings demonstrate that P2Y(2) receptor mediates TF expression in HCAEC through new mechanisms involving Src/p38 and Rho/JNK pathways, possibly contributing to a pro-thrombotic status after vascular injury.

Indexed as

Gene Expression RegulationMAP Kinase Signaling SystemAdenosine TriphosphateAntinematodal AgentsCell Line, TumorCoronary VesselsEndothelial CellsHumansMitogen-Activated Protein Kinase KinasesNF-kappa BReceptors, Purinergic P2Receptors, Purinergic P2Y2SuraminThromboplastinUridine TriphosphateAdenosine TriphosphateAntinematodal AgentsMitogen-Activated Protein Kinase KinasesNF-kappa BP2RY11 protein, humanReceptors, Purinergic P2Receptors, Purinergic P2Y2SuraminThromboplastinUridine Triphosphate

Identifiers

PMID21652710
PMCPMC3143661
OpenAlexW2071739144

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.