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Cells
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Platelet Function beyond Hemostasis
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Platelet Function beyond Hemostasis

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (30 August 2021) | Viewed by 24634

Special Issue Editor

Dr. Peter Bugert

E-Mail Website
Guest Editor
Institute of Transfusion Medicine and Immunology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Friedrich-Ebert-Str. 107, D-68167 Mannheim, Germany
Interests: basic research on the molecular and functional characterization of receptors and adapter proteins involved in platelet adhesion; clinical research on patients with inherited and immune-mediated platelet function disorders; basic and clinical research on platelets in tumor progression

Special Issue Information

Dear Colleagues,

Blood platelets are well-known for their essential role in hemostasis and thrombus formation. In the context of infection, the inflammatory and thrombotic mechanisms are closely related and affect each other. This process has been introduced as thrombo-inflammation. It significantly contributes to the control of infection and pathogen spread. Not only in infection, but also in other inflammatory diseases, thrombotic mechanisms and the role of platelets are perceived. Furthermore, platelet granules contain numerous different proteins known to be involved not only in hemostasis and inflammation, but also in angiogenesis, wound healing, and tumor growth. The adhesion of platelets to other cells and matrix proteins via specific receptors followed by activation of the platelets is a central mechanism leading to the release of the granules content. In this way, platelets play a significant role in many different processes beyond hemostasis, including angiogenesis and tumor progression.

The aim of this Special Issue is to provide an overview of the current knowledge on platelets affecting inflammation, innate immune response, vascular development, wound healing and vice versa. Furthermore, aspects of tumor growth and progression are considered for a better understanding of platelet function beyond hemostasis.

Dr. Peter Bugert
Guest Editor

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Keywords

  • platelets
  • innate immunity
  • inflammation
  • thrombo-inflammation
  • angiogenesis
  • vascular biology
  • tumor progression
  • circulating tumor cells
  • metastasis

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Published Papers (4 papers)

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Research

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9 pages, 742 KiB  
Article
A Novel Likely Pathogenic Variant in the BLOC1S5 Gene Associated with Hermansky-Pudlak Syndrome Type 11 and an Overview of Human BLOC-1 Deficiencies
by Doris Boeckelmann, Mira Wolter, Barbara Käsmann-Kellner, Udo Koehler, Lea Schieber-Nakamura and Barbara Zieger
Cells 2021, 10(10), 2630; https://doi.org/10.3390/cells10102630 - 1 Oct 2021
Cited by 8 | Viewed by 2463
Abstract
Hermansky-Pudlak syndrome (HPS) is a heterogeneous disorder combining oculocutaneous albinism (OCA) and a platelet function disorder of varying severity as its most prominent features. The genes associated with HPS encode for different BLOC- (biogenesis of lysosome-related organelles complex) complexes and for the AP-3 [...] Read more.
Hermansky-Pudlak syndrome (HPS) is a heterogeneous disorder combining oculocutaneous albinism (OCA) and a platelet function disorder of varying severity as its most prominent features. The genes associated with HPS encode for different BLOC- (biogenesis of lysosome-related organelles complex) complexes and for the AP-3 (adaptor protein-3) complex, respectively. These proteins are involved in maturation, trafficking, and the function of lysosome-related organelles (LROs) such as melanosomes and platelet δ-granules. Some patients with different types of HPS can develop additional complications and symptoms like pulmonary fibrosis, granulomatous colitis, and immunodeficiency. A new type of HPS has recently been identified associated with genetic alterations in the BLOC1S5 gene, which encodes the subunit Muted of the BLOC-1 complex. Our aim was to unravel the genetic defect in two siblings with a suspected HPS diagnosis (because of OCA and bleeding symptoms) using next generation sequencing (NGS). Platelet functional analysis revealed reduced platelet aggregation after stimulation with ADP and a severe secretion defect in platelet δ-granules. NGS identified a novel homozygous essential splice site variant in the BLOC1S5 gene present in both affected siblings who are descendants of a consanguine marriage. The patients exhibited no additional symptoms. Our study confirms that pathogenic variants of BLOC1S5 cause the recently described HPS type 11. Full article
(This article belongs to the Special Issue Platelet Function beyond Hemostasis)
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Review

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16 pages, 1997 KiB  
Review
Platelet Activation Mechanisms and Consequences of Immune Thrombocytopenia
by Siyu Sun, Rolf T. Urbanus, Hugo ten Cate, Philip G. de Groot, Bas de Laat, Johan W. M. Heemskerk and Mark Roest
Cells 2021, 10(12), 3386; https://doi.org/10.3390/cells10123386 - 1 Dec 2021
Cited by 40 | Viewed by 11120
Abstract
Autoimmune disorders are often associated with low platelet count or thrombocytopenia. In immune-induced thrombocytopenia (IIT), a common mechanism is increased platelet activity, which can have an increased risk of thrombosis. In addition, or alternatively, auto-antibodies suppress platelet formation or augment platelet clearance. Effects [...] Read more.
Autoimmune disorders are often associated with low platelet count or thrombocytopenia. In immune-induced thrombocytopenia (IIT), a common mechanism is increased platelet activity, which can have an increased risk of thrombosis. In addition, or alternatively, auto-antibodies suppress platelet formation or augment platelet clearance. Effects of the auto-antibodies are linked to the unique structural and functional characteristics of platelets. Conversely, prior platelet activation may contribute to the innate and adaptive immune responses. Extensive interplay between platelets, coagulation and complement activation processes may aggravate the pathology. Here, we present an overview of the reported molecular causes and consequences of IIT in the most common forms of autoimmune disorders. These include idiopathic thrombocytopenic purpura (ITP), systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), drug-induced thrombocytopenia (DITP), heparin-induced thrombocytopenia (HIT), COVID-19 vaccine-induced thrombosis with thrombocytopenia (VITT), thrombotic thrombocytopenia purpura (TTP), and hemolysis, the elevated liver enzymes and low platelet (HELLP) syndrome. We focus on the platelet receptors that bind auto-antibodies, the immune complexes, damage-associated molecular patterns (DAMPs) and complement factors. In addition, we review how circulating platelets serve as a reservoir of immunomodulatory molecules. By this update on the molecular mechanisms and the roles of platelets in the pathogenesis of autoimmune diseases, we highlight platelet-based pathways that can predispose for thrombocytopenia and are linked thrombotic or bleeding events. Full article
(This article belongs to the Special Issue Platelet Function beyond Hemostasis)
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15 pages, 1183 KiB  
Review
Platelets in ITP: Victims in Charge of Their Own Fate?
by Vivianne S. Nelson, Anne-Tess C. Jolink, Sufia N. Amini, Jaap Jan Zwaginga, Tanja Netelenbos, John W. Semple, Leendert Porcelijn, Masja de Haas, Martin R. Schipperus and Rick Kapur
Cells 2021, 10(11), 3235; https://doi.org/10.3390/cells10113235 - 19 Nov 2021
Cited by 17 | Viewed by 4252
Abstract
Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder. The pathophysiological mechanisms leading to low platelet levels in ITP have not been resolved, but at least involve autoantibody-dependent and/or cytotoxic T cell mediated platelet clearance and impaired megakaryopoiesis. In addition, T cell imbalances involving [...] Read more.
Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder. The pathophysiological mechanisms leading to low platelet levels in ITP have not been resolved, but at least involve autoantibody-dependent and/or cytotoxic T cell mediated platelet clearance and impaired megakaryopoiesis. In addition, T cell imbalances involving T regulatory cells (Tregs) also appear to play an important role. Intriguingly, over the past years it has become evident that platelets not only mediate hemostasis, but are able to modulate inflammatory and immunological processes upon activation. Platelets, therefore, might play an immuno-modulatory role in the pathogenesis and pathophysiology of ITP. In this respect, we propose several possible pathways in which platelets themselves may participate in the immune response in ITP. First, we will elaborate on how platelets might directly promote inflammation or stimulate immune responses in ITP. Second, we will discuss two ways in which platelet microparticles (PMPs) might contribute to the disrupted immune balance and impaired thrombopoiesis by megakaryocytes in ITP. Importantly, from these insights, new starting points for further research and for the design of potential future therapies for ITP can be envisioned. Full article
(This article belongs to the Special Issue Platelet Function beyond Hemostasis)
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12 pages, 562 KiB  
Review
Reticulated Platelets—Which Functions Have Been Established by In Vivo and In Vitro Data?
by Muataz Ali Hamad, Nancy Schanze, Nicolas Schommer, Thomas Nührenberg and Daniel Duerschmied
Cells 2021, 10(5), 1172; https://doi.org/10.3390/cells10051172 - 12 May 2021
Cited by 9 | Viewed by 5604
Abstract
Reticulated platelets (RP) are the youngest platelet fraction released into the circulation. These immature platelets have increased RNA content, a larger cell volume, more dense granules, higher levels of surface activation markers and are thought to be more reactive compared to their mature [...] Read more.
Reticulated platelets (RP) are the youngest platelet fraction released into the circulation. These immature platelets have increased RNA content, a larger cell volume, more dense granules, higher levels of surface activation markers and are thought to be more reactive compared to their mature counterparts. RP have been associated with cardiovascular disease, diabetes and increased mortality. Yet only a few animal studies investigating RP have been conducted so far and further investigations are warranted. Established methods to count RP are flow cytometry (staining with thiazole orange or SYTO13) or fully automated hematology analyzers (immature platelet fraction, IPF). IPF has been established as a diagnostic parameter in thrombocytopenia, cardiovascular disease and, in particular, the response to antiplatelet therapy. This review seeks to provide an overview of the key features of RP as well as preanalytical and analytical aspects that need to be considered when working with this platelet population. Full article
(This article belongs to the Special Issue Platelet Function beyond Hemostasis)
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