What is the clinical evidence from this study?

Study design: Other. Population: COX-2 deficiency. Intervention: COX-2 gene deletion vs. Wild-type (WT). Primary outcome: Platelet function and megakaryopoiesis.

January 1, 2015Thrombosis and Haemostasis

Abnormal megakaryopoiesis and platelet function in cyclooxygenase-2-deficient mice

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Key result

COX-2 deletion in mice delays bone marrow megakaryopoiesis, promoting compensatory splenic megakaryocyte hyperplasia and the release of hyper-responsive platelets with increased thrombogenicity.

Population

COX-2-/- mice (10-12 weeks old and 28 weeks old)

Comparison

COX-2 gene deletion (COX-2-/-) and splenectomy vs Wild-type (WT) mice

Design

Preclinical

Authors

PAPatrizia AmadioCentro Cardiologico Monzino BRBianca RoccaLUM Jean Monnet University MPMaurizio PesceCross-Cutting Cardiology

Discussion

Member takes

Implication

Findings should not alter COX-2 inhibitor use; hypothesis-generating for human megakaryopoiesis and thrombosis risk.

Structured PICO

Population

COX-2-/- mice (10-12 weeks old and 28 weeks old) compared to wild-type mice to analyze the effect of COX-2 deficiency on megakaryopoiesis and platelet function.

Exposure

COX-2 gene deletion (COX-2-/-) and splenectomy

Comparator

Wild-type (WT) mice

Outcome

Megakaryopoiesis and platelet function (including aggregation, TXA2 biosynthesis, CD62P and CD41/CD61 expression, platelet-fibrinogen binding, and thromboembolic death after collagen/epinephrine injection)surrogate

COX-2 deletion in mice delays bone marrow megakaryopoiesis, leading to compensatory splenic hyperplasia and the release of hyper-responsive, pro-thrombotic platelets.

Cite This Study

Amadio et al. (2015) studied COX-2 deficiency. COX-2 gene deletion vs. Wild-type (WT) was evaluated on Platelet function and megakaryopoiesis. COX-2 deletion in mice delays bone marrow megakaryopoiesis, promoting compensatory splenic megakaryocyte hyperplasia and the release of hyper-responsive platelets with increased thrombogenicity.

synapsesocial.com/papers/6a91a613850905e91d03441d https://doi.org/10.1160/th14-10-0872

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January 1, 2015Thrombosis and Haemostasis

Abnormal megakaryopoiesis and platelet function in cyclooxygenase-2-deficient mice

View Full Paper

Ask AI

Bookmark

Key result

COX-2 deletion in mice delays bone marrow megakaryopoiesis, promoting compensatory splenic megakaryocyte hyperplasia and the release of hyper-responsive platelets with increased thrombogenicity.

Population

COX-2-/- mice (10-12 weeks old and 28 weeks old)

Comparison

COX-2 gene deletion (COX-2-/-) and splenectomy vs Wild-type (WT) mice

Design

Preclinical

Authors

PAPatrizia AmadioCentro Cardiologico Monzino BRBianca RoccaLUM Jean Monnet University MPMaurizio PesceCross-Cutting Cardiology

Discussion

Member takes

Implication

Findings should not alter COX-2 inhibitor use; hypothesis-generating for human megakaryopoiesis and thrombosis risk.

Structured PICO

Population

COX-2-/- mice (10-12 weeks old and 28 weeks old) compared to wild-type mice to analyze the effect of COX-2 deficiency on megakaryopoiesis and platelet function.

Exposure

COX-2 gene deletion (COX-2-/-) and splenectomy

Comparator

Wild-type (WT) mice

Outcome

COX-2 deletion in mice delays bone marrow megakaryopoiesis, leading to compensatory splenic hyperplasia and the release of hyper-responsive, pro-thrombotic platelets.

Cite This Study

synapsesocial.com/papers/6a91a613850905e91d03441d https://doi.org/10.1160/th14-10-0872

Also Consider

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

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