ArticleBlood2014
Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Jak2 V617F clonal hematopoiesis promotes arterial thrombosis via platelet activation and cross talk.Blood · 2024Pooled it
- Fufang Huangbo Formula mitigates myeloproliferative neoplasms by activating p53/p21 signaling axis and inhibiting STAT3 and NF-κB signaling pathways.Pharmaceutical science advances · 2026Article
- Exacerbation of thromboinflammation by JAK2V617F mutation worsens the prognosis of cerebral venous sinus thrombosis.Blood advances · 2024Article
- Blood cell JAKtivation aggravates cerebral venous thrombosis.Blood advances · 2024Article
- Neutrophil-specific expression of JAK2-V617F or CALRmut induces distinct inflammatory profiles in myeloproliferative neoplasia.Journal of hematology & oncology · 2024Article
- Multiomic profiling reveals metabolic alterations mediating aberrant platelet activity and inflammation in myeloproliferative neoplasms.The Journal of clinical investigation · 2024Article
- Practical management of the haemorrhagic complications of myeloproliferative neoplasms.British journal of haematology · 2022Review
- Hematopoiesis of Indeterminate Potential and Atherothrombotic Risk.Thrombosis and haemostasis · 2022Review
- Thromboinflammation in Myeloproliferative Neoplasms (MPN)-A Puzzle Still to Be Solved.International journal of molecular sciences · 2022Review
- Neutrophil-to-lymphocyte ratio is a novel predictor of venous thrombosis in polycythemia vera.Blood cancer journal · 2022Article
- Bleeding diathesis in mice lacking JAK2 in platelets.Blood advances · 2021Article
- Novel Pathophysiological Mechanisms of Thrombosis in Myeloproliferative Neoplasms.Current hematologic malignancy reports · 2021Review
- Article
- Pathogenesis of cardiovascular events in BCR-ABL1-negative myeloproliferative neoplasms.Leukemia · 2021Review
- Platelet Dysfunction and Thrombosis in JAK2Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm.The Journal of clinical investigation · 2020Article
- N-acetylcysteine inhibits thrombosis in a murine model of myeloproliferative neoplasm.Blood advances · 2020Article
- Quantitative Optical Diffraction Tomography Imaging of Mouse Platelets.Frontiers in physiology · 2020Article
- Review
- Emerging Factors Implicated in Fibrotic Organ-Associated Thrombosis: The Case of Two Organs.TH open : companion journal to thrombosis and haemostasis · 2019Review
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombosis is common in patients suffering from myeloproliferative neoplasm (MPN), whereas bleeding is less frequent. JAK2(V617F), the main mutation involved in MPN, is considered as a risk factor for thrombosis, although the direct link between the mutation and hemostatic disorders is not strictly established. We investigated this question using conditional JAK2(V617F) knock-in mice with constitutive and inducible expression of JAK2(V617F) in hematopoietic cells, which develop a polycythemia vera (PV)-like disorder evolving into myelofibrosis. In vitro, thrombosis was markedly impaired with an 80% decrease in platelet-covered surface, when JAK2(V617F) blood was perfused at arterial shear over collagen. JAK2(V617F) platelets presented only a moderate glycoprotein (GP) VI deficiency not responsible for the defective platelet accumulation. In contrast, a decreased proportion of high-molecular-weight von Willebrand factor multimers could reduce platelet adhesion. Accordingly, the tail bleeding time was prolonged. In the FeCl3-induced thrombosis model, platelet aggregates formed rapidly but were highly unstable. Interestingly, vessels were considerably dilated. Thus, mice developing PV secondary to constitutive JAK2(V617F) expression exhibit a bleeding tendency combined with the accelerated formation of unstable clots, reminiscent of observations made in patients. Hemostatic defects were not concomitant with the induction of JAK2(V617F) expression, suggesting they were not directly caused by the mutation but were rather the consequence of perturbations in blood and vessel homeostasis.
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