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New Aspects of Platelets in Physiology and Pathology from Their Birth to Their Death

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 20407

Special Issue Editor

Dr. Alexandre Kauskot

E-Mail Website
Guest Editor
HITh, UMR-S 1176, INSERM—Faculty of Medicine, University Paris-Saclay, F-94270 Le Kremlin-Bicêtre, France
Interests: platelets; microplatelets; macroplatelets; thrombocytopenia; β-galactose

Special Issue Information

Dear Colleagues, 

The amount of platelets in the blood is the net result of the production of platelets and their elimination. In human blood, the reference values for the number of platelets are between 150 and 400 G / L and their lifespan is approximately 10 days. It is important that the production and clearance of platelets remain in balance, since thrombocytopenia or the presence of non-functioning platelets can increase the risk of bleeding. By contrast, thrombocytosis and/or abnormal platelet activation can trigger clot formation and increase the risk of thrombosis. Platelets are produced by hematopoietic cells called megakaryocytes (MK) and once mature, the megakaryocyte can form blood platelets. Different actors such as the medullary environment (matrix and cells), cytokines, transcription factors, and the reorganization of the cell's cytoskeleton regulate those process. Once in the circulation, platelets are directly involved, under physiological conditions, in the arrest of bleeding by formation of the hemostatic plug and, under pathological conditions, in the development of thrombosis. Multiple processes regulate their haemostatic function, involving various combinations of ligands, receptors, cytoskeleton and signaling molecules. The lifespan of platelets in circulation is brief, close to 10 days in humans and in a healthy individual, and the majority of platelets are not consumed by hemostatic processes. Little was known about the physiological mechanisms involved in platelet clearance until fairly recently. This elimination of platelets occurs either by consumption of platelets and/or by the mechanism of desialylation or loss of sialic acid on the platelet surface. Currently, new platelet disorders, inherited and acquired, have been reported with impaired platelet formation, function and/or clearance that either cosegregate with a predicted disease-causing gene variant or are associated with pathogenic mechanisms such as chronic liver disease, sepsis, cancer, COVID-19 and autoimmune disorder (immune thrombocytopenia, systemic lupus erythematosus, etc.). Answering questions related to platelet dysfunction will be important for obtaining a better understanding of their physiology, and will guide future efforts to correct the platelet count and function in patients.

Dr. Alexandre Kauskot
Guest Editor

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Keywords

  • platelets
  • bleeding
  • thrombocytopenia
  • mutations
  • clearance
  • cytoskeleton
  • platelet function

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Published Papers (5 papers)

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Research

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16 pages, 2673 KiB  
Article
SHIP1 Controls Internal Platelet Contraction and αIIbβ3 Integrin Dynamics in Early Platelet Activation
by Sonia Severin, Alessandra Consonni, Gaëtan Chicanne, Sophie Allart, Bernard Payrastre and Marie-Pierre Gratacap
Int. J. Mol. Sci. 2023, 24(2), 958; https://doi.org/10.3390/ijms24020958 - 4 Jan 2023
Cited by 2 | Viewed by 1619
Abstract
The Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1) is known to dephosphorylate PtdIns(3,4,5)P3 into PtdIns(3,4)P2 and to interact with several signaling proteins though its docking functions. It has been shown to negatively regulate platelet adhesion and spreading on a fibrinogen [...] Read more.
The Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1) is known to dephosphorylate PtdIns(3,4,5)P3 into PtdIns(3,4)P2 and to interact with several signaling proteins though its docking functions. It has been shown to negatively regulate platelet adhesion and spreading on a fibrinogen surface and to positively regulate thrombus growth. In the present study, we have investigated its role during the early phase of platelet activation. Using confocal-based morphometric analysis, we found that SHIP1 is involved in the regulation of cytoskeletal organization and internal contractile activity in thrombin-activated platelets. The absence of SHIP1 has no significant impact on thrombin-induced Akt or Erk1/2 activation, but it selectively affects the RhoA/Rho-kinase pathway and myosin IIA relocalization to the cytoskeleton. SHIP1 interacts with the spectrin-based membrane skeleton, and its absence induces a loss of sustained association of integrins to this network together with a decrease in αIIbβ3 integrin clustering following thrombin stimulation. This αIIbβ3 integrin dynamics requires the contractile cytoskeleton under the control of SHIP1. RhoA activation, internal platelet contraction, and membrane skeleton integrin association were insensitive to the inhibition of PtdIns(3,4,5)P3 synthesis or SHIP1 phosphatase activity, indicating a role for the docking properties of SHIP1 in these processes. Altogether, our data reveal a lipid-independent function for SHIP1 in the regulation of the contractile cytoskeleton and integrin dynamics in platelets. Full article
(This article belongs to the Special Issue New Aspects of Platelets in Physiology and Pathology from Their Birth to Their Death)
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13 pages, 2449 KiB  
Article
High-frequency Contactless Sensor for the Detection of Heparin-Induced Thrombocytopenia Antibodies via Platelet Aggregation
by Nida Zaman Khan, Daniel Martin, Uwe Pliquett, Yahor Zaikou, Nacke Thomas, Doris Heinrich, J. Michael Köhler and Thi-Huong Nguyen
Int. J. Mol. Sci. 2022, 23(22), 14395; https://doi.org/10.3390/ijms232214395 - 19 Nov 2022
Cited by 3 | Viewed by 1913
Abstract
Heparin-induced thrombocytopenia (HIT), a severe autoimmune disorder, occurs in patients undergoing heparin therapy. The presence of platelet-activating antibodies against platelet factor 4/Heparin in the blood confirms patients suffering from HIT. The most widely used methods for HIT diagnosis are immunoassays but the results [...] Read more.
Heparin-induced thrombocytopenia (HIT), a severe autoimmune disorder, occurs in patients undergoing heparin therapy. The presence of platelet-activating antibodies against platelet factor 4/Heparin in the blood confirms patients suffering from HIT. The most widely used methods for HIT diagnosis are immunoassays but the results only suit to rule out HIT as the assays provide only around 50% specificity. To confirm HIT, samples with positive results in immunoassays are retested in functional assays (>98% specificity) that track platelet-activating antibodies via platelet aggregation. However, the protocols in functional assays are either time-consuming (due to the requirement of the detection of serotonin release) or require highly trained staff for the visualization of platelets. Here, we applied a cheap and easy-to-use contactless sensor, which employs high-frequency microwaves to detect the changes in the resonant frequency caused by platelet aggregation/activation. Analysis of change in conductivity and permittivity allowed us to distinguish between HIT-like (KKO) and non-HIT-like (RTO) antibodies. KKO caused a stronger reduction of conductivity of platelet samples than RTO. Our results imply that the high-frequency contactless sensor can be a promising approach for the development of a better and easier method for the detection of HIT. Full article
(This article belongs to the Special Issue New Aspects of Platelets in Physiology and Pathology from Their Birth to Their Death)
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16 pages, 2270 KiB  
Article
Platelet Hemostasis Reactions at Different Temperatures Correlate with Intracellular Calcium Concentration
by Igor Mindukshev, Ekaterina Fock, Irina Dobrylko, Julia Sudnitsyna, Stepan Gambaryan and Mikhail A. Panteleev
Int. J. Mol. Sci. 2022, 23(18), 10667; https://doi.org/10.3390/ijms231810667 - 14 Sep 2022
Cited by 9 | Viewed by 3327
Abstract
Hypo- and hyperthermia affect both primary and secondary hemostasis; however, there are controversial data concerning platelet activation and the underlying mechanisms under hypo- and hyperthermia. The discrepancies in the data could be partly explained by different approaches to hemostatic reactions analysis. We applied [...] Read more.
Hypo- and hyperthermia affect both primary and secondary hemostasis; however, there are controversial data concerning platelet activation and the underlying mechanisms under hypo- and hyperthermia. The discrepancies in the data could be partly explained by different approaches to hemostatic reactions analysis. We applied a new LaSca-TMF laser particle analyzer for a simultaneous fluorescence and laser scattering analysis of platelet responses at different temperatures. Human platelets were activated by ADP in a wide range of temperatures, and platelet transformations (e.g., a shape change reaction, aggregation and clot formation) and the intracellular calcium concentration ([Ca2+]i) were analyzed by LaSca-TMF and confocal microscopy. The platelet shape change reaction gradually increased with a rising temperature. The platelet aggregation strongly decreased at low ADP concentrations with the augmentation of the temperature and was independent of the temperature at high ADP concentrations. In contrast, the clotting time decreased with a temperature increase. Similar to the aggregation response, a rise in [Ca2+]i triggered by low ADP concentrations was higher under hypothermic conditions and the differences were independent of the temperature at high ADP concentrations. We showed that the key reactions of cellular hemostasis are differentially regulated by temperature and demonstrated for the first time that an accelerated aggregation under hypothermic conditions directly correlated with an increased level in [Ca2+]i in platelets. Full article
(This article belongs to the Special Issue New Aspects of Platelets in Physiology and Pathology from Their Birth to Their Death)
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17 pages, 4993 KiB  
Article
Pannexin-1 Activation by Phosphorylation Is Crucial for Platelet Aggregation and Thrombus Formation
by Lisa Maria Metz and Margitta Elvers
Int. J. Mol. Sci. 2022, 23(9), 5059; https://doi.org/10.3390/ijms23095059 - 2 May 2022
Cited by 8 | Viewed by 2781
Abstract
Pannexin-1 (PANX1) is a transmembrane protein that forms ion channels as hexamers on the plasma membrane. Electrophysiological studies prove that PANX1 has a high conductance for adenosine triphosphate (ATP), which plays an important role as a signal molecule in platelet activation. Recently, it [...] Read more.
Pannexin-1 (PANX1) is a transmembrane protein that forms ion channels as hexamers on the plasma membrane. Electrophysiological studies prove that PANX1 has a high conductance for adenosine triphosphate (ATP), which plays an important role as a signal molecule in platelet activation. Recently, it was shown that PANX1 channels modulate platelet functions. To date, it remains unclear how PANX1 channels are activated and which signaling mechanisms are responsible for impaired hemostasis and thrombosis. Analysis of PANX1 phosphorylation at Tyr198 and Tyr308, and the impact on platelet activation and thrombus formation using genetically modified platelets or pharmacological inhibitors. Platelet activation via immunoreceptor tyrosine-based activation motif (ITAM) coupled, G Protein-Coupled Receptors (GPCR) and thromboxane receptor (TP)-mediated signaling pathways led to increased PANX1 phosphorylation at Tyr198 and Tyr308. We identified the Src-GPVI signaling axes as the main pathway inducing PANX1 activation, while PKC and Akt play a minor role. PANX1 channels function as ATP release channels in platelets to support arterial thrombus formation. PANX1 activation is regulated by phosphorylation at Tyr198 and Tyr308 following platelet activation. These results suggest an important role of PANX1 in hemostasis and thrombosis by releasing extracellular ATP to support thrombus formation. Full article
(This article belongs to the Special Issue New Aspects of Platelets in Physiology and Pathology from Their Birth to Their Death)
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Review

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15 pages, 689 KiB  
Review
The Analysis of the Human Megakaryocyte and Platelet Coding Transcriptome in Healthy and Diseased Subjects
by Koenraad De Wispelaere and Kathleen Freson
Int. J. Mol. Sci. 2022, 23(14), 7647; https://doi.org/10.3390/ijms23147647 - 11 Jul 2022
Cited by 8 | Viewed by 10003
Abstract
Platelets are generated and released into the bloodstream from their precursor cells, megakaryocytes that reside in the bone marrow. Though platelets have no nucleus or DNA, they contain a full transcriptome that, during platelet formation, is transported from the megakaryocyte to the platelet. [...] Read more.
Platelets are generated and released into the bloodstream from their precursor cells, megakaryocytes that reside in the bone marrow. Though platelets have no nucleus or DNA, they contain a full transcriptome that, during platelet formation, is transported from the megakaryocyte to the platelet. It has been described that transcripts in platelets can be translated into proteins that influence platelet response. The platelet transcriptome is highly dynamic and has been extensively studied using microarrays and, more recently, RNA sequencing (RNA-seq) in relation to diverse conditions (inflammation, obesity, cancer, pathogens and others). In this review, we focus on bulk and single-cell RNA-seq studies that have aimed to characterize the coding transcriptome of healthy megakaryocytes and platelets in humans. It has been noted that bulk RNA-seq has limitations when studying in vitro-generated megakaryocyte cultures that are highly heterogeneous, while single-cell RNA-seq has not yet been applied to platelets due to their very limited RNA content. Next, we illustrate how these methods can be applied in the field of inherited platelet disorders for gene discovery and for unraveling novel disease mechanisms using RNA from platelets and megakaryocytes and rare disease bioinformatics. Next, future perspectives are discussed on how this field of coding transcriptomics can be integrated with other next-generation technologies to decipher unexplained inherited platelet disorders in a multiomics approach. Full article
(This article belongs to the Special Issue New Aspects of Platelets in Physiology and Pathology from Their Birth to Their Death)
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