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Molecular Research on Platelet Function in Disease 2.0
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Molecular Research on Platelet Function in Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 June 2023) | Viewed by 8804

Special Issue Editor

Dr. Eleni Gavriilaki

E-Mail Website
Guest Editor
Second Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece
Interests: hematologic malignancies; thrombosis; complement; cellular therapy; lymphoma; myeloma; COVID-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Platelets are anucleated constituents of blood that are not only crucial for hemostasis but also involved in the pathophysiology of several cardiovascular and neurovascular diseases in addition to immunological and inflammatory processes. Recently, investigations on the molecular processes underlying platelet function have revealed that platelets are more complex than previously anticipated. Indeed, the well-known platelet responses to a blood vessel wall consisting of adhesion, secretion of granule contents, and aggregation require rapid and progressive changes in platelet form and function, which are orchestrated downstream by specific receptors on the platelet surface as well as intracellular molecular pathways. Despite knowledge of numerous molecular mediators pivotal to platelet function, it remains unclear how signals from multiple platelet receptors coordinate platelet responses in specific disease settings.

This Special Issue will focus on molecular mechanisms underlying platelet response and function in clinical diseases. The aim is to integrate the latest research on platelet biogenesis, activation, and aggregation, focusing on the molecular pathways involved in the dysregulation of important molecular players affecting platelet biology and thereby resulting in different diseases.

Contributions on these and related topics are welcome, including original research and review articles. We particularly welcome submissions from postdocs, PhD students, and young researchers.

Dr. Eleni Gavriilaki
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • thrombosis
  • bleeding, receptors
  • signal transductions
  • oxidative stress
  • antiplatelet drugs
  • inflammation
  • microparticles

Related Special Issue

Published Papers (4 papers)

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Research

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13 pages, 2209 KiB  
Article
Regulation of Glycoprotein VI-Dependent Platelet Activation and Thrombus Formation by Heparan Sulfate Proteoglycan Perlecan
by Isabella Provenzale, Ilaria De Simone, Jonathan M. Gibbins, Johan W. M. Heemskerk, Paola E. J. van der Meijden and Chris I. Jones
Int. J. Mol. Sci. 2023, 24(17), 13352; https://doi.org/10.3390/ijms241713352 - 28 Aug 2023
Cited by 3 | Viewed by 1001
Abstract
Proteoglycans form a heterogeneous family of proteins with covalently bound sulfated glycosaminoglycans. The extracellular matrix proteoglycan perlecan has been proposed to bind to the platelet- and megakaryocyte-specific receptor G6bB, co-regulating platelet glycoprotein VI (GPVI) signaling. The derived non-sulfate proteoglycan endorepellin was previously shown [...] Read more.
Proteoglycans form a heterogeneous family of proteins with covalently bound sulfated glycosaminoglycans. The extracellular matrix proteoglycan perlecan has been proposed to bind to the platelet- and megakaryocyte-specific receptor G6bB, co-regulating platelet glycoprotein VI (GPVI) signaling. The derived non-sulfate proteoglycan endorepellin was previously shown to enhance platelet adhesion via the collagen receptor, integrin α2β1. Here, we compared the roles of perlecan and other matrix proteoglycans in platelet responses and thrombus formation. We used multi-color flow cytometry to measure the degranulation and integrin αIIbβ3 activation of washed platelets in response to various proteoglycans and collagen-related peptide (CRP), the GPVI agonist. Perlecan, but not endorepellin, enhanced the CRP-induced activation of platelets in a time- and concentration-dependent manner. Similar to collagen, immobilized perlecan, but not other proteoglycans, supported static platelet adhesion and spreading. In-flowed whole-blood perlecan diminished shear-dependent platelet adhesion, while it enforced GPVI-dependent thrombus formation—to a larger extent than endorepellin—to induce more contracted aggregates of activated platelets. We concluded that the sulfated proteoglycan perlecan enhances GPVI-dependent platelet responses extending to thrombus formation, but it does so at the expense of reduced adhesion of platelets under flow. Full article
(This article belongs to the Special Issue Molecular Research on Platelet Function in Disease 2.0)
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11 pages, 2062 KiB  
Article
Recombinant ADAMTS-13 Improves Survival of Mice Subjected to Endotoxemia
by Daniel Gao, Zhou Zhou, Ruidong Ma, Huaizhu Wu, Trung Nguyen, Li Liu and Jingfei Dong
Int. J. Mol. Sci. 2023, 24(14), 11782; https://doi.org/10.3390/ijms241411782 - 22 Jul 2023
Cited by 2 | Viewed by 959
Abstract
When stimulated by proinflammatory mediators, endothelial cells release ultra-large von Willebrand factor (ULVWF) multimers that are hyperactive in activating and aggregating platelets. These ULVWF multimers can accumulate in the circulation and on the inflamed endothelium because they are insufficiently cleaved by the metalloprotease [...] Read more.
When stimulated by proinflammatory mediators, endothelial cells release ultra-large von Willebrand factor (ULVWF) multimers that are hyperactive in activating and aggregating platelets. These ULVWF multimers can accumulate in the circulation and on the inflamed endothelium because they are insufficiently cleaved by the metalloprotease ADAMTS-13, which becomes moderately deficient under conditions of systemic inflammation. This moderate ADAMTS-13 deficiency may lead to thrombotic complications that contribute to ischemic tissue injury and organ failure that are associated with severe infections. To test this hypothesis, we investigated whether recombinant ADAMTS-13 improves the pathological course of endotoxemia in lipopolysaccharide (LPS)-treated mice. C57BL/J6 mice received a bolus infusion of either 5 µg/mouse of ADAMTS-13 or vehicle control 30 min after LPS challenge and were monitored for seven-day survival. During the monitoring period, platelet counts, VWF antigen, and ADAMTS-13 activity were measured. Thrombosis was also examined by the immunohistochemistry in the liver. We found that ADAMTS-13 reduced mortality from 66% to 34.9%. The improved survival was associated with a greater recovery from thrombocytopenia, higher plasma ADAMTS-13 activity, and less thrombotic vascular occlusion. These results suggest that systemic inflammation could result in deficient ULVWF proteolysis by ADAMTS-13 and that ADAMTS-13 improves the outcomes of endotoxemia-induced inflammation. Full article
(This article belongs to the Special Issue Molecular Research on Platelet Function in Disease 2.0)
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18 pages, 2387 KiB  
Article
Chronic Immune Platelet Activation Is Followed by Platelet Refractoriness and Impaired Contractility
by Izabella A. Andrianova, Alina I. Khabirova, Anastasia A. Ponomareva, Alina D. Peshkova, Natalia G. Evtugina, Giang Le Minh, Timur B. Sibgatullin, John W. Weisel and Rustem I. Litvinov
Int. J. Mol. Sci. 2022, 23(13), 7336; https://doi.org/10.3390/ijms23137336 - 30 Jun 2022
Cited by 7 | Viewed by 2265
Abstract
Autoimmune diseases, including systemic lupus erythematosus (SLE), have a high risk of thrombotic and hemorrhagic complications associated with altered platelet functionality. We studied platelets from the blood of SLE patients and their reactivity. The surface expression of phosphatidylserine, P-selectin, and active integrin αIIbβ3 [...] Read more.
Autoimmune diseases, including systemic lupus erythematosus (SLE), have a high risk of thrombotic and hemorrhagic complications associated with altered platelet functionality. We studied platelets from the blood of SLE patients and their reactivity. The surface expression of phosphatidylserine, P-selectin, and active integrin αIIbβ3 were measured using flow cytometry before and after platelet stimulation. Soluble P-selectin was measured in plasma. The kinetics of platelet-driven clot contraction was studied, as well as scanning and transmission electron microscopy of unstimulated platelets. Elevated levels of membrane-associated phosphatidylserine and platelet-attached and soluble P-selectin correlated directly with the titers of IgG, anti-dsDNA-antibodies, and circulating immune complexes. Morphologically, platelets in SLE lost their resting discoid shape, formed membrane protrusions and aggregates, and had a rough plasma membrane. The signs of platelet activation were associated paradoxically with reduced reactivity to a physiological stimulus and impaired contractility that revealed platelet exhaustion and refractoriness. Platelet activation has multiple pro-coagulant effects, and the inability to fully contract (retract) blood clots can be either a hemorrhagic or pro-thrombotic mechanism related to altered clot permeability, sensitivity of clots to fibrinolysis, obstructiveness, and embologenicity. Therefore, chronic immune platelet activation followed by secondary platelet dysfunction comprise an understudied pathogenic mechanism that supports hemostatic disorders in autoimmune diseases, such as SLE. Full article
(This article belongs to the Special Issue Molecular Research on Platelet Function in Disease 2.0)
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Review

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15 pages, 2762 KiB  
Review
Severe Trauma-Induced Coagulopathy: Molecular Mechanisms Underlying Critical Illness
by Christian Zanza, Tatsiana Romenskaya, Fabrizio Racca, Eduardo Rocca, Fabio Piccolella, Andrea Piccioni, Angela Saviano, George Formenti-Ujlaki, Gabriele Savioli, Francesco Franceschi and Yaroslava Longhitano
Int. J. Mol. Sci. 2023, 24(8), 7118; https://doi.org/10.3390/ijms24087118 - 12 Apr 2023
Cited by 5 | Viewed by 3906
Abstract
Trauma remains one of the leading causes of death in adults despite the implementation of preventive measures and innovations in trauma systems. The etiology of coagulopathy in trauma patients is multifactorial and related to the kind of injury and nature of resuscitation. Trauma-induced [...] Read more.
Trauma remains one of the leading causes of death in adults despite the implementation of preventive measures and innovations in trauma systems. The etiology of coagulopathy in trauma patients is multifactorial and related to the kind of injury and nature of resuscitation. Trauma-induced coagulopathy (TIC) is a biochemical response involving dysregulated coagulation, altered fibrinolysis, systemic endothelial dysfunction, platelet dysfunction, and inflammatory responses due to trauma. The aim of this review is to report the pathophysiology, early diagnosis and treatment of TIC. A literature search was performed using different databases to identify relevant studies in indexed scientific journals. We reviewed the main pathophysiological mechanisms involved in the early development of TIC. Diagnostic methods have also been reported which allow early targeted therapy with pharmaceutical hemostatic agents such as TEG-based goal-directed resuscitation and fibrinolysis management. TIC is a result of a complex interaction between different pathophysiological processes. New evidence in the field of trauma immunology can, in part, help explain the intricacy of the processes that occur after trauma. However, although our knowledge of TIC has grown, improving outcomes for trauma patients, many questions still need to be answered by ongoing studies. Full article
(This article belongs to the Special Issue Molecular Research on Platelet Function in Disease 2.0)
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