Study decodes blood-clotting mechanism
Here’s some hope for those who dread getting a nick, because their blood just refuses to clot.
In a medical breakthrough, Harvard University researchers have decoded the molecular mechanism that determines how the body decides how much clotting is optimum to close a fresh wound.
Dr Wesley Wong, the lead author of the study from the Rowland Institute at Harvard University, said, “The human body has an incredible ability to heal from life's scrapes and bruises. A central aspect of this response to damage is the ability to bring bleeding to an end, a process known as haemostasis. Yet regulating haemostasis is a complex balancing act.”
This regulation is very important because too much clotting could lead to thrombosis, a condition that could turn fatal, and too little could bleed a person to death.The research team found that when an injury is detected in the body, certain miniscule forces are unleashed in the blood stream and are picked up by a molecular ‘sensor’ in the A2 region on the Von Willebrand factor (VWF), a protein required for platelets to stick to each other to form a clot. This sensor then gives signals to the VWF, which unfolds, allowing an enzyme called ADAMTS13 to cut it into smaller pieces. The size of the cut VWF decides how much clotting is essential to close a particular wound.
“In the body, these cutting events decrease haemostatic potential and also enable blood clots to be trimmed in size. The system is so finely tuned that the A2 shear sensor is able to regulate the size of VWF within blood stream – maintaining the optimal size for responding to traumas,” Wong said.
While the mechanism works like a finely tuned machine in normal humans, it doesn’t in those suffering from coagulation diseases such as Von Willebrand disease (VWD), thrombotic thrombocytopenic purpura (TTP) and haemolytic-uraemic syndrome.
VWD, the most common blood-clotting disease, is usually inherited but can also be caused by other conditions. The disorder involves a faulty VWF and causes nosebleeds and easy bruising in mild cases and heavy internal bleeding in severe ones. It can even cause heart failure.
The other disorder, TTP, is caused by the faulty release of ADAMTS13. Under this condition, a number of microscopic clots are formed in the blood stream and can even damage certain organs. Haemolytic-uraemic syndrome is characterised by low platelet count, anaemia and possibly renal failure.
