By Sofia Öling
PhD student at TREC
The formation of a blood clot (a thrombus) in a blood vessel disturbs the normal blood flow, and if the vessel is completely blocked it can lead to necrosis, or cell death. The platelet cells in your body play a crucial role in the formation of clots. If you are healthy, the rate between coagulation and anticoagulation is in balance. This means that, when you need clot formation, for instance if you get a small cut or a scrub wound, your blood will form a clot to stop the bleeding, but it will not form more than necessary.
In a rare blood cancer, called essential thrombocythemia (ET), this balance between coagulation and anticoagulation is disturbed. The patients suffering from this disease have an increased production of platelets, making the balance skewed to the procoagulant side. The patients therefore have a higher risk of thrombosis in their veins, the vessels that bring deoxygenated blood back to the heart and lungs. As their production of platelets is increased, these patients have higher risk of thrombosis.
The platelets in ET patients express a protein on their surface, which means that they can be distinguished from healthy platelets. Normally such platelets are removed by macrophages, the white blood cells of the immune system that remove foreign particles or infected cells from the body. However, these patients have so many sick platelets that the macrophages cannot keep up in the removal process.
A group of scientists from China has conducted a study where they show that endothelial cells, which line the inner walls of all blood vessels, can “eat” the platelets in these patients. Once the endothelial cells have recognized a sick platelet, they can remove the platelet by phagocytosis (eating/absorbing it).
The scientists marked the platelets and endothelial cells with specific labels and were able to study the events under microscope. They could see that after incubating the two different cell types together for 1.5 hour, the endothelial cells had phagocytosed the platelets. This proved that in a laboratory setting, the endothelial cells could distinguish between sick and healthy platelets, and then remove the sick ones.
Their study shows a novel mechanism to remove sick platelets from ET patients, which could be useful to prevent thrombosis in these patients. However, further research is needed as this was only shown in a laboratory setting and not in actual patients.
Reference: Ji, S, Dong, W, Qi, Y, et al. Phagocytosis by endothelial cells inhibits procoagulant activity of platelets of essential thrombocythemia in vitro. J Thromb Haemost. (2019).
