Platelet heterogeneity: variety makes immune and vascular function better

Abstract

Abstract Platelets are dynamic cells that perform vital roles both in thrombosis and in immune regulation. Platelets are activated through well described signaling pathways after injury to the vascular wall to prevent excess bleeding and initiate vascular repair. However, platelet functions extend beyond this initial physical phase of platelet activation through their expression and secretion of angiogenic factors and immune mediators that initiate wound healing and recruit leukocytes to prevent infection. Not only do activated platelets induce inflammation and vascular repair but circulating resting platelets maintain vascular integrity and immune homeostasis. Furthermore, many studies have shown that platelets are not homogenous, demonstrating transcriptomic and proteomic differences that associate with platelet phenotypes and functions in multiple disease states. Platelets are produced by megakaryocytes that are found not only in the bone marrow but also in the lungs and spleen. Megakaryocytes within the bone marrow are heterogeneous, which may contribute to platelet heterogeneity. In addition, unlike the megakaryocytes in other tissues, lung megakaryocytes are immune differentiated and proportionately produce more platelets at times of increased demand, perhaps adding to the platelet heterogeneity in disease contexts. In this review, we will discuss the underlying mechanisms that may lead to the platelet heterogeneity that impact both health maintenance and disease.