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June 13, 2011Journal of Clinical InvestigationOpen Access

P2rx7-/- mice were protected from TF-dependent FeCl3-induced carotid artery thrombosis, and P2X7 receptor signaling induced activation of TF procoagulant activity and release of TF+ MPs.

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Why the study?

Does P2X7 receptor signaling contribute to tissue factor-dependent thrombosis in mice?

Population

Mouse models including P2rx7-/- mice, bone marrow chimeras, and mouse myeloid cells (macrophages and SMCs)

Comparison

Genetic deletion of P2X7 receptor or anti-PDI… vs Wild-type mice or control conditions

Design

Preclinical

Authors

CFChristian Furlan-FreguiaPMPatrizia MarcheseAGAndrás Gruber

Discussion

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Overview

P2X7 signaling may promote TF-dependent thrombosis in mice; leaves open its viability as an antithrombotic target in humans.

Structured PICO

Does P2X7 receptor signaling contribute to tissue factor-dependent thrombosis in mice?

P
Population
Mouse models including P2rx7-/- mice, bone marrow chimeras, and mouse myeloid cells (macrophages and SMCs)
I
Intervention
Genetic deletion of P2X7 receptor (P2rx7-/-) or anti-PDI antibody administration
C
Comparator
Wild-type mice or control conditions
O
Outcome
Tissue factor-dependent FeCl3-induced carotid artery thrombosis and release of procoagulant microparticlessurrogate

PDI regulates a P2X7 receptor-dependent signaling pathway that generates prothrombotic tissue factor, linking inflammation and thrombosis and providing a potential new target for antithrombotic therapy.

Cite This Study

Furlan-Freguia et al. (2011) studied this question.

synapsesocial.com/papers/6a71a43735aa2c282ce2da57https://doi.org/10.1172/jci46129
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Also Consider

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  4. 4Lysine residues 165 and 166 are essential for the cofactor function of tissue factor.1991 · 53 citations
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