Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
August 1, 2003Journal of Clinical Investigation

P2Y12 regulates platelet adhesion/activation, thrombus growth, and thrombus stability in injured arteries

View Full Paper
Ask AI
Bookmark
Share

Key result

P2Y12 deficiency in mice significantly delayed the time to first thrombus and prevented arterial occlusion (P < 0.0001), demonstrating its critical role in platelet adhesion, activation, and thrombus stability.

Why the study?

Does the complete absence of the P2Y12 receptor impair platelet adhesion, activation, thrombus growth, and stability in injured arteries?

Population

P2Y12-null mice generated by a gene-targeting strategy on a mixed 129/Sv and C57BL/6J background, along with…

Comparison

Genetic deletion of the P2Y12 receptor (P2Y12-/-). vs Wild-type and heterozygous littermates.

Design

Preclinical, Genotyping was performed after the bleeding time study by an…

Authors

PAPatrick AndréSDSuzanne M. DelaneyTLThomas J. LaRocca

Discussion

Loading...

Member takes

Overview

P2Y12 deficiency impairs thrombosis in mice; hypothesis-generating for aggressive antagonism without aspirin, pending human validation.

Structured PICO

Does the complete absence of the P2Y12 receptor impair platelet adhesion, activation, thrombus growth, and stability in injured arteries?

P
Population
P2Y12-null mice (10-13 weeks old) were evaluated to determine the role of the P2Y12 receptor in platelet thrombosis using in vivo and ex vivo models.
E
Exposure
Genetic deletion of the P2Y12 receptor (P2Y12-/-).
C
Comparator
Wild-type (WT) and heterozygous (P2Y12+/-) littermates.
O
Outcome
In vivo arterial thrombogenesis (time for appearance of first thrombus, thrombus stability, and time to occlusion) following FeCl3-induced mesenteric artery injury.surrogate

Main Result

p-value: p=<0.0001

Complete deficiency of P2Y12 in mice impairs multiple steps of thrombosis including platelet adhesion, activation, and thrombus stability, suggesting aggressive P2Y12 antagonism may be effective without aspirin.

Limitations

  • Subtle differences exist between murine and human P2Y12 activities, such as the lack of dense-granule release in mouse platelets compared with humans.

Cite This Study

André et al. (2003) studied Arterial thrombosis. P2Y12 deficiency vs. Wild-type mice was evaluated on Time for occlusion of mesenteric arteries (p=<0.0001). P2Y12 deficiency in mice significantly delayed the time to first thrombus and prevented arterial occlusion (P < 0.0001), demonstrating its critical role in platelet adhesion, activation, and thrombus stability.

synapsesocial.com/papers/6a94331a2167e799456d3473https://doi.org/10.1172/jci200317864
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Molecular identification and characterization of the platelet ADP receptor targeted by thienopyridine antithrombotic drugs2001 · 417 citations
  2. 2Effects of adenosine 5′-diphosphate (ADP) receptor blockade on platelet aggregation under flow2002 · 21 citations
  3. 3Optimal Antagonism of GPIIb/IIIa Favors Platelet Adhesion by Inhibiting Thrombus Growth1996 · 30 citations
  4. 4Identification of P2Y12-dependent and -independent mechanisms of glycoprotein VI–mediated Rap1 activation in platelets2003 · 80 citations
  5. 5Pro-coagulant state resulting from high levels of soluble P-selectin in blood2000 · 320 citations