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Published on: June 29, 2015
A mouse model to study thrombotic complications of thalassemia
Yosef Kalish1, Zeev Malyutin1, Ela Shai1
1Coagulation Unit, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Abstract:
Patients with β-thalassemia major and mainly intermedia have an increased risk for developing venous and arterial thrombosis which may be related to circulating pathological red blood cells (RBC) and continuous platelet activation. In the present study we used a modified thalassemic mice model in conjunction with a "real-time" carotid thrombus formation procedure to investigate thrombotic complications of thalassemia. Heterozygous Th3/+ mice, which lack one copy of their β-major and β-minor globin genes, exhibit anomalies in RBC size and shape, chronic anemia and splenomegaly which recapitulate the phenotype of human β-thalassemia intermedia. Flow cytometry measurements showed higher reactive oxygen species generation, indicating oxidative stress, in platelets and RBC of the thalassemic mice compared with wild type mice concomitant with an increase in reduced glutathione content which may represent a compensatory response to oxidative stress, and exposed phosphatidylserine which indicates platelet activation. To elucidate the effect of thalassemia on the development of arterial thrombosis, we studied photochemical-induced real-time thrombus formation in the carotid artery of these mice. The results indicated a significantly shorter "time to occlusion" in the thalassemic mice compared to wild type mice, which was prolonged following in vivo aspirin treatment. We suggest that this mouse model may contribute to our understanding of platelet activation and the hypercoagulable state in thalassemia and lay foundations to screening of anti-platelet drugs as well as anti-oxidants as possible therapeutics for prevention of thrombosis in thalassemia patients.
Insights
Thalassemia patients experience increased thrombosis risk due to red blood cell (RBC) abnormalities and platelet activation. A new mouse model shows accelerated clot formation, highlighting potential therapeutic targets like anti-platelet drugs and antioxidants.
Area of Science:
- Hematology
- Vascular Biology
- Thrombosis Research
Background:
- Patients with beta-thalassemia major and intermedia exhibit heightened risk of venous and arterial thrombosis.
- This increased thrombotic risk is potentially linked to circulating pathological red blood cells (RBCs) and sustained platelet activation.
Purpose of the Study:
- To investigate the thrombotic complications of thalassemia using a modified mouse model.
- To elucidate the impact of thalassemia on arterial thrombosis development and evaluate potential therapeutic interventions.
Main Methods:
- Utilized heterozygous Th3/+ mice, exhibiting RBC anomalies, anemia, and splenomegaly, mimicking human beta-thalassemia intermedia.
- Employed flow cytometry to assess oxidative stress, glutathione levels, and platelet activation markers (phosphatidylserine exposure) in thalassemic mice.
- Investigated real-time carotid artery thrombus formation using a photochemical-induced method in thalassemic and wild-type mice, assessing the effect of aspirin treatment.
Main Results:
- Thalassemic mice displayed increased reactive oxygen species generation and phosphatidylserine exposure on platelets and RBCs, indicating oxidative stress and platelet activation.
- A significantly shorter time to carotid artery occlusion was observed in thalassemic mice compared to wild-type controls.
- In vivo aspirin treatment effectively prolonged the time to occlusion in the thalassemic mouse model.
Conclusions:
- The Th3/+ mouse model effectively recapitulates key aspects of thalassemia, including RBC pathology and hypercoagulability.
- This model provides a valuable platform for understanding platelet activation and the hypercoagulable state in thalassemia.
- The findings support the potential of anti-platelet drugs and antioxidants as therapeutic strategies for preventing thrombosis in thalassemia patients.
