Targeting a key step in blood clotting, towards a new anticoagulant medicine

Defining the GPVI-dimer-fibrin interaction in collagen-independent, thrombus formation

When we have a cut the body responds by forming a blood clot at the wound site. Platelets are small blood cells that prevent excessive bleeding when a blood vessel is injured, by clumping together and forming a blood clot. Blood clots are stabilized by a molecule called fibrin and are dissolved when the vessel is healed. But the formation of blood clots in the wrong place at the wrong time can be fatal. These clots can break-off and travel in the blood circulation and block blood vessels in the brain, causing stroke, or in the heart, resulting in a heart attack. Dr Stephanie Jung and her team suspect that a structure present at the surface of the platelet called GPVI-dimer can interact with fibrin and could play a role in disease states. In this project, they will study how GPVI-dimer binds fibrin and how this can stabilise fibrin clots, to find ways to prevent or minimize this interaction and stop unwanted clot formation. They will also make antibodies to stop the action of GPVI-dimer and to measure it in patients. This study might identify GPVI-dimer as a potential marker of disease state and/or a target for future treatment to prevent stroke and heart attacks, while leaving the body’s vital healing response unhindered.