Production and Destruction of Platelets

Platelet counts in blood are controlled by the rates of their production by megakaryocytes and the kinetics of their removal. Alterations in either process can lead to thrombocytopenia (TCP) or thrombocytosis. Under conditions of TCP, the spleen and liver are the sites for accelerated platelet destruction, and in thrombocytosis, the spleen can become a supplemental breeding ground for megakaryocytes, in addition to the bone marrow space. Humans produce and remove 1011 platelets per day. Senile or damaged platelets are detected as such and are removed from blood. Platelets must also be removed locally at diverse sites where they have discovered vascular damage, attached and become activated to prevent blood leakage. The mechanism of this local removal in the blood vascular system is not well described or understood. The removal of platelets from flowing blood mandates a system that detects changes that accu‐ mulate in the platelet surface with age and that responds by binding and removing the platelets when changes reach a critical level. Surface changes must either increase the availability of clearance ligands or remove anti-clearance signals such as CD47 [1]. Changes in the platelet surface that signal for removal include phosphatidylserine upregulation, deglycosylation of membrane glycoproteins, in particular Gp1bα of the vWf receptor, and Ig binding. Diseases that accelerate removal arbitrate their impact at the platelet surface.