Heyu Ni- disponible en anglais seulement
Disponible en anglais seulement
Senior Scientist
Canadian Blood Services
Platform Director and Scientist for Hematology, Cancer and Immunological Diseases
Keenan Research Centre for Biomedical Science – St. Michael's Hospital
Professor
Laboratory Medicine and Pathobiology – University of Toronto
Medicine – University of Toronto
Physiology – University of Toronto
Formation
- Doctor of Philosophy, University of Manitoba
- MD, Anhui Medical University, China
- Master of Science, Anhui Medical University, China
Publications
Hemostasis and Thrombosis - finding the right balance
A complex system of cells, proteins and signaling molecules in the blood and blood vessels maintain a delicate balance between bleeding (hemostasis) and clotting (thrombosis). Dr. Heyu Ni’s laboratory investigates the role(s) of adhesion molecules involved in clot formation and their implications for hemostasis (including bleeding disorders) and thrombotic diseases (including heart attack and stroke).
Why is this important?
Understanding the cellular and molecular mechanisms of hemostasis and thrombotic diseases could lead to the development of new therapies as well as diagnostic tools to control bleeding disorders and cardiovascular diseases, such as heart attack and stroke, which are the leading cause of mortality and morbidity worldwide.
While completing his post-doctoral fellowship at Harvard, Dr. Heyu Ni established an intravital microscopy thrombosis model to study thrombus formation in real time in live mice. Through direct monitoring of platelet adhesion and aggregation in vivo, the group was the first to observe that platelet aggregation and thrombus formation still occur in mice lacking both von Willebrand factor (VWF) and fibrinogen (Fg), two proteins previously thought to be essential for thrombus formation. This surprising discovery challenged the established theory of thrombosis and suggested that other unidentified molecule(s) were also involved in thrombosis and hemostasis and may provide novel targets for anti-thrombotic therapies. Dr. Ni’s team is in the process of identifying these mystery molecules using several state-of-the-art techniques such as proteomics and confocal intravital microscopy. In particular, the work focuses on the role of adhesion molecules such as the beta3 integrin (e.g. GPIIbIIIa) and GPIb alpha complexes.
Hemostasis and Thrombosis - finding the right balance
A complex system of cells, proteins and signaling molecules in the blood and blood vessels maintain a delicate balance between bleeding (hemostasis) and clotting (thrombosis). Dr. Heyu Ni’s laboratory investigates the role(s) of adhesion molecules involved in clot formation and their implications for hemostasis (including bleeding disorders) and thrombotic diseases (including heart attack and stroke).
Why is this important?
Understanding the cellular and molecular mechanisms of hemostasis and thrombotic diseases could lead to the development of new therapies as well as diagnostic tools to control bleeding disorders and cardiovascular diseases, such as heart attack and stroke, which are the leading cause of mortality and morbidity worldwide.
While completing his post-doctoral fellowship at Harvard, Dr. Heyu Ni established an intravital microscopy thrombosis model to study thrombus formation in real time in live mice. Through direct monitoring of platelet adhesion and aggregation in vivo, the group was the first to observe that platelet aggregation and thrombus formation still occur in mice lacking both von Willebrand factor (VWF) and fibrinogen (Fg), two proteins previously thought to be essential for thrombus formation. This surprising discovery challenged the established theory of thrombosis and suggested that other unidentified molecule(s) were also involved in thrombosis and hemostasis and may provide novel targets for anti-thrombotic therapies. Dr. Ni’s team is in the process of identifying these mystery molecules using several state-of-the-art techniques such as proteomics and confocal intravital microscopy. In particular, the work focuses on the role of adhesion molecules such as the beta3 integrin (e.g. GPIIbIIIa) and GPIb alpha complexes.
Understanding Diseases to Optimize Transfusion Practice
Dr. Heyu Ni’s laboratory studies allo- and auto-immune diseases related to bleeding disorders such as immune thrombocytopenia (ITP) and fetal and neonatal alloimmune thrombocytopenic purpura (FNAIT). These diseases are characterized by the presence of antibodies that target platelet antigens and result in a loss of platelets, which in turn can lead to uncontrolled bleeding and, in rare cases, death.
Why is this important?
These studies help us understand immune diseases and their treatment and could lead to more appropriate clinical practice of both diagnosis and treatment.
While ITP and FNAITP are characterized by immune-mediated destruction of platelets, how and why these diseases occur isn’t clear. Dr. Ni’s group has investigated how ITP mediated by anti-beta3 integrin (GPIIbIIIa) and anti-GPIb antibodies differ, and have found that these two antibody specificities may respond to therapy differently. The group recently conducted a retrospective study in adults with ITP and concluded that patients with autoantibodies targeting the platelet surface protein GPIIb/IIIa respond well to intravenous immunoglobulin G (IVIG) and steroid therapies, but those with autoantibodies targeting platelet GPIb/IX do not. This has important implications for human ITP and potential screening of patients in order to successfully treat this disease. IVIG, which is provided to Canadian physicians by Canadian Blood Services, is limited in supply and is an expensive treatment option. A better understanding of the mechanism by which IVIG works and development of alternative therapies to IVIG would benefit patients and the blood system in general.
Dr. Ni’s group developed the first animal model of FNAIT, characterizing the disease and its response to IVIG therapy. Currently, the laboratory is studying the molecular and cellular basis of ITP, the maternal immune responses to fetal platelet antigens and the roles of anti-angiogenesis and apoptosis in the pathogenesis of FNAIT.