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The mechanisms regulating expression and function of surface receptors on blood platelets are critical for understanding cardiovascular diseases involving aberrant platelet function, not only thrombotic diseases such as heart attack or stroke, but other pathology involving platelets including coagulopathy and autoimmune thrombocytopenia caused by anti-platelet antibodies. Improved diagnosis and therapeutic targeting of platelet-specific receptors mediating arterial thrombosis can save many lives ....The mechanisms regulating expression and function of surface receptors on blood platelets are critical for understanding cardiovascular diseases involving aberrant platelet function, not only thrombotic diseases such as heart attack or stroke, but other pathology involving platelets including coagulopathy and autoimmune thrombocytopenia caused by anti-platelet antibodies. Improved diagnosis and therapeutic targeting of platelet-specific receptors mediating arterial thrombosis can save many lives given the prevalence and severity of disease.Read moreRead less
Investigation Of The Role For GPVI In Platelet Function And Thrombosis
Funder
National Health and Medical Research Council
Funding Amount
$542,772.00
Summary
Blood cells play an important role in maintaining healthy blood vessels. We are studying the role of platelets in blood clots following vessel injury. However, while critical for normal blood vessel maintenance, these cells also contribute to diseases including thrombosis. We will examine how an important platelet receptor called GPVI promotes blood clot formation, and examine whether combining anticoagulant drugs with GPVI deficient platelets leads to a more effective anticlotting approach.
Investigation Of A Novel Role For Factor XIII In Regulating The Adhesive Function Of Platelets
Funder
National Health and Medical Research Council
Funding Amount
$243,000.00
Summary
Platelets are small specialised blood cells that are extremely important for the normal formation of blood clots and for the repair of injured blood vessels. We are studying the processes that allow platelets to stick to the site of vessel injury and to each other to form stable blood clots. If this process proceeds unchecked, harmful blood clots can form which block blood vessels and cause heart attacks and strokes. There are many factors, both inside and outside platelets, which control how bi ....Platelets are small specialised blood cells that are extremely important for the normal formation of blood clots and for the repair of injured blood vessels. We are studying the processes that allow platelets to stick to the site of vessel injury and to each other to form stable blood clots. If this process proceeds unchecked, harmful blood clots can form which block blood vessels and cause heart attacks and strokes. There are many factors, both inside and outside platelets, which control how big and how fast a blood clot grows and whether it becomes harmful enough to cause a blood vessel blockage. One of these factors is the level of platelet 'stickiness' or 'reactivity'. We are working towards a better understanding of how platelet reactivity is regulated. Specifically, we believe we have identified a new factor which keeps blood clots at a size that is not harmful to cause blood vessel blockade. This information will not only increase our knowledge of blood clot formation in health and disease but also may help in the development of new therapies for the prevention of heart attack and stroke.Read moreRead less
Investigation Of Mechanotransduction Mechanisms In Platelets
Funder
National Health and Medical Research Council
Funding Amount
$481,500.00
Summary
Platelets are extremely important cells that stop bleeding by sticking to injured blood vessel walls, forming blood clots. Excessive clotting can lead to fatal vascular events such as heart attack and stroke. On the other hand, defects in blood clotting can result in life threatening bleeding problems. Platelets stick to sites of vessel wall injury through the interaction between cell surface receptors and sticky materials (proteins) that become exposed to the blood flow when the vessel wall is ....Platelets are extremely important cells that stop bleeding by sticking to injured blood vessel walls, forming blood clots. Excessive clotting can lead to fatal vascular events such as heart attack and stroke. On the other hand, defects in blood clotting can result in life threatening bleeding problems. Platelets stick to sites of vessel wall injury through the interaction between cell surface receptors and sticky materials (proteins) that become exposed to the blood flow when the vessel wall is damaged. The stickiness of platelets is controlled by many proteins (and-or enzymes) inside these blood cells. These proteins transmit messages from platelet receptors on the surface into the cell interior, thereby controlling platelet behaviour. We are in the process of identifying several types of proteins-enzymes which are responsible for controlling platelet stickiness. The studies proposed in this application will provide better understanding of the complicated pathways regulating platelet stickiness and clot formation. The knowledge gained may utimately assist in the design of specific drugs for the prevention and-or treatment of heart attacks and strokes.Read moreRead less
Investigation Of Negative Signalling Mechanisms In Platelets
Funder
National Health and Medical Research Council
Funding Amount
$292,500.00
Summary
Platelets are specialised blood cells essential for normal blood clotting. We are studying the processes that control platelets sticking to the exposed vessel wall, to each other and to other cells to form a stable blood clot at the site of injury to stop bleeding. The same processes, when unchecked, could lead to the formation of harmful large blood clots that may block blood vessels in the heart or brain, resulting in heart attack or stroke. Platelets stick to the blood vessel wall and each ot ....Platelets are specialised blood cells essential for normal blood clotting. We are studying the processes that control platelets sticking to the exposed vessel wall, to each other and to other cells to form a stable blood clot at the site of injury to stop bleeding. The same processes, when unchecked, could lead to the formation of harmful large blood clots that may block blood vessels in the heart or brain, resulting in heart attack or stroke. Platelets stick to the blood vessel wall and each other through sticky proteins called receptors on the cell surface. Receptors are able to bind to their specific ligands such as von Willebrand factor (vWf) and collagen which become exposed following vessel wall damage. The interaction between the ligands and receptors will trigger many biochemical changes within platelets, called signal transduction, that control platelet stickiness. The aim of this research project is to investigate the signalling processes that are utilised by the major platelet receptor called integrin alpha IIb beta 3. We are particularly interested in identifying the negative signalling process utilised by this receptor to dampen the positive signals required for platelet stickiness, to achieve a balanced clotting process. The identification of these specific signalling pathways will not only increase our knowledge of blood clot formation in health and disease, but also help develop potential new therapies for the prevention of heart diseases and strokes.Read moreRead less
Zbtb11 is a druggable protein that is mis-expressed in blood cancers - second biggest cause of cancer death in Australia - and liver cancer, third leading cause of death from cancer worldwide. We have found that it interacts with 2 other proteins with potential roles in these diseases. Our studies examine the nature of these Zbtb11-partner interactions and their particular consequences for blood disorders. Zbtb11 contributions to disease development will be a target for novel disease therapy.
The Role Of Med12, A Subunit Of RNA Polymerase II Mediator, In Haemopoiesis
Funder
National Health and Medical Research Council
Funding Amount
$495,490.00
Summary
In a screen of zebrafish for mutations in blood cell development, we isolated a mutant called syrah. The mutation causing the blood defect was identified in a gene called med12, which encodes a component of the RNA transcription machinery in cells. To understand how this mutation causes a reduction in blood cells, we will identify the proteins that interact with the med12 protein. Understanding the pathway involved may lead to the discovery of new causes of human congenital blood diseases.
Platelet Receptor Regulation In Autoimmune Disease
Funder
National Health and Medical Research Council
Funding Amount
$507,536.00
Summary
In response to bleeding, blood platelets use receptors to form a thrombus (blood clot) and block further loss of blood and aid tissue repair. People treated with heparin prior to surgery, can form autoantibodies that attack platelets, leading to thombus and thrombocytopenia (dangerous loss of circulating platelets). This is a significant clinical problem that is difficult to diagnose. We will determine how platelet receptor shedding can aid the diagnosis of heparin-induced thrombocytopenia.
Antibody-mediated Dendritic Cell Depletion To Attenuate GVHD
Funder
National Health and Medical Research Council
Funding Amount
$434,510.00
Summary
Not all patients with leukemia will be cured by chemotherapy. Stem cell transplantation improves their chances of survival. Stem cell transplantation requires intensive chemotherapy and radiotherapy to eradicate the underlying disease and infusion of healthy stem cells to provide an anti-leukemic effect and normal blood cells. Recovery from transplantation is not straightforward. Recovery can be hampered by the immunological reaction of the donor cells against the patient (Graft versus Host Dise ....Not all patients with leukemia will be cured by chemotherapy. Stem cell transplantation improves their chances of survival. Stem cell transplantation requires intensive chemotherapy and radiotherapy to eradicate the underlying disease and infusion of healthy stem cells to provide an anti-leukemic effect and normal blood cells. Recovery from transplantation is not straightforward. Recovery can be hampered by the immunological reaction of the donor cells against the patient (Graft versus Host Disease [GVHD]), despite immunosuppression. GVHD produces serious damage to the internal organs and lining of the mouth and gut. Recovery can also be circumvented by leukemic relapse. GVHD is associated with an increased risk of death and dying after transplantation. To date therapy for GVHD has relied on eliminating the T cells that cause the disease. However for T cells to cause damage they must first be primed with antigen presented on activated dendritic cells. The intensive conditioning therapy required to eradicate the underlying disease before transplantation also activates dendritic cells. Our project seeks to investigate the effects of lethal and non-lethal conditioning on dendritic cells with the aim of validating the use of antibodies designed to deplete activated dendritic cells as therapy for graft versus host disease.Read moreRead less