2021; 41(3): 318-322
Ann Lab Med 2019; 39(4): 343-344
Published online July 1, 2019 https://doi.org/10.3343/alm.2019.39.4.343
Copyright © Korean Society for Laboratory Medicine.
Expanded Impacts of Platelet Functions: Beyond Hemostasis and Thrombosis
1Department of Laboratory Medicine, Kyung Hee University Hospital, Seoul, Korea; 2Department of Laboratory Medicine, Konkuk University School of Medicine, Seoul, Korea
Correspondence to: Sun Young Cho https://orcid.org/0000-0002-3208-5446
Department of Laboratory Medicine, School of Medicine, Kyung Hee University Hospital, 23 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea, Tel: +82-2-958-8671, Fax: +82-2-958-8609
Mina Hur https://orcid.org/0000-0002-4429-9978
Department of Laboratory Medicine, Konkuk University School of Medicine, Konkuk University Medical Center, 120-1 Neungdong-ro, Gwangjin-gu, Seoul 05030, Korea, Tel: +82-2-2030-5581, Fax: +82-2-2636-6764
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Platelets are very small (2 µm) anucleate hematologic effector cells  with a lifespan of approximately 8–10 days . Platelets are traditionally well known for their primary functions in thrombosis and hemostasis . The hemostasis function was first identified by Osler in 1873, who described platelets as a “blood plaque” in the white thrombus . In physiologic states, platelets are not accessible to subendothelial structures such as collagen fibers or von-Willebrand factor . However, when the vessel wall is injured, the subendothelial structures are exposed, resulting in the initiation of platelet adhesion [3,4]. This interaction consequently triggers signal cascades in platelets to seal the thrombus leak at the site of vascular injury . Thus, platelets have long been simply regarded as the main components of bleeding control [3,4]. In addition to this primary role of preventing blood loss from an injured vessel, the thrombus prevents the dissemination of foreign pathogens into the organism .
Beyond their fundamental roles in primary hemostasis, platelets serve as essential elements of the immune system and pro-inflammatory reaction [4,5]. Recent evidence has been accumulated to support the crucial functions of platelets in various diseases, including inflammation, infection, and malignancy [2,6,7]. Owing to their surface adhesion molecules and receptors that can recognize and bind to the endothelium, leukocytes, or circulating pathogens [3,4], platelets also play important roles in vasomotor function and chemotaxis  by activating circulating leukocytes to perform their immunologic functions .
Activated platelets release highly active microparticles and form pseudopods on their surfaces that promote their interactions with neutrophils, lymphocytes, and other immune cells, as well as platelet–platelet bonds . Among these interactions, the circulating neutrophils are largely responsible for potentiating the thromboinflammatory ability of activated platelets . This phenomenon has been widely reported in high-grade inflammatory diseases such as rheumatoid arthritis [2,6]. Moreover, various kinds of tumor-related cytokines have been shown to influence megakaryopoiesis and thrombopoiesis in malignancies . Platelet reactivity is mainly determined by megakaryopoiesis through the action of thrombopoietin (TPO) , and a TPO-dependent mechanism was suggested as one of the key links between platelets and cancer [1,9,10]. For example, TPO may be produced by ovarian and hepatocellular cancer cells, and elevated TPO levels enhance the production of platelets and their differentiation [9,10,11].
In this issue of
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