What is the clinical evidence from this study?

Study design: Other. Population: Thrombosis and Hemostasis (n=123). Intervention: P2Y1 receptor knockout vs. Wild-type (P2Y1+/+). Primary outcome: Bleeding time (seconds) (p=<0.0001).

What does this research mean for the field?

Targeted disruption of the P2Y1 receptor in mice significantly prolongs bleeding time and reduces mortality from acute thromboembolism by 50%, demonstrating its essential role in thrombosis and its potential as an antithrombotic drug target. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research investigates the role of the P2Y(1) receptor in platelet aggregation and thrombotic resistance.

December 15, 1999Journal of Clinical InvestigationOpen Access

Defective platelet aggregation and increased resistance to thrombosis in purinergic P2Y1 receptor–null mice

Q: What are the key findings of this study?

Targeted disruption of the P2Y1 receptor in mice significantly prolonged bleeding time (225.7 vs 126.6 seconds, p<0.0001) and reduced mortality from acute thromboembolism by 50%.

Q: What does this research mean for the field?

Targeted disruption of the P2Y1 receptor in mice significantly prolongs bleeding time and reduces mortality from acute thromboembolism by 50%, demonstrating its essential role in thrombosis and its potential as an antithrombotic drug target. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

This research investigates the role of the P2Y(1) receptor in platelet aggregation and thrombotic resistance.

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Key result

Targeted disruption of the P2Y1 receptor in mice significantly prolonged bleeding time (225.7 vs 126.6 seconds, p<0.0001) and reduced mortality from acute thromboembolism by 50%.

Why the study?

Does genetic deletion of the P2Y(1) receptor prevent thromboembolism in mice?

Population

P2Y(1)-null mice and wild-type mice

Comparison

Genetic deletion of the P2Y(1) receptor vs Wild-type mice

Design

Preclinical

Authors

CLCatherine LéonInserm BHBéatrice HechlerInserm MFMonique FreundMayo Clinic in Arizona

Discussion

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Implication

P2Y1 deletion may increase bleeding while halving thromboembolism mortality in mice; leaves open its viability as an antithrombotic target.

Key Points

This research investigates the role of the P2Y(1) receptor in platelet aggregation and thrombotic resistance.
Generated P2Y(1)-null mice to assess platelet function in response to ADP and other agonists.
Analyzed platelet aggregation under varying concentrations of ADP and additional thrombotic agents.
Examined the effects on thrombosis following intravenous injection of ADP or collagen and adrenaline.
P2Y(1)-null mice exhibit defective platelet aggregation in response to ADP, with high ADP concentrations inducing aggregation without shape change.
Platelets from P2Y(1)-deficient mice show impaired aggregation to other agonists and maintain adenylyl cyclase inhibition, indicating an alternative ADP receptor.
P2Y(1)-null mice do not have spontaneous bleeding but are resistant to thromboembolism induced by ADP, collagen, and adrenaline.

Structured PICO

Does genetic deletion of the P2Y(1) receptor prevent thromboembolism in mice?

Population

P2Y(1)-null mice and wild-type mice

Intervention

Genetic deletion of the P2Y(1) receptor

Comparator

Wild-type mice

Outcome

Platelet aggregation in response to ADP and resistance to thromboembolismsurrogate

Main Result

Absolute Event Rate: 225.7% vs 126.6%

p-value: p=<0.0001

The P2Y(1) receptor is essential for ADP-induced platelet aggregation and thrombosis, identifying it as a potential target for novel antithrombotic drugs.

Limitations

The role of the P2Y1 receptor in the early phase of collagen-induced platelet activation requires further characterization.
Further studies are needed to characterize the intracellular pathways involved when the P2cyc receptor is activated independently of the P2Y1 receptor.

Cite This Study

Léon et al. (1999) studied Thrombosis and Hemostasis (n=123). P2Y1 receptor knockout vs. Wild-type (P2Y1+/+) was evaluated on Bleeding time (seconds) (p=<0.0001). Targeted disruption of the P2Y1 receptor in mice significantly prolonged bleeding time (225.7 vs 126.6 seconds, p<0.0001) and reduced mortality from acute thromboembolism by 50%.

synapsesocial.com/papers/6a1c55fcbc71fb1015a96d0f https://doi.org/10.1172/jci8399

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Implication

P2Y1 deletion may increase bleeding while halving thromboembolism mortality in mice; leaves open its viability as an antithrombotic target.

Defective platelet aggregation and increased resistance to thrombosis in purinergic P2Y1 receptor–null mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Limitations

Cite This Study

Defective platelet aggregation and increased resistance to thrombosis in purinergic P2Y1 receptor–null mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

Also Consider