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Biomedicines
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Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic...
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Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1767

Special Issue Editor

Dr. Henry Nording

E-Mail Website
Guest Editor
1. Cardioimmunology Group, Medical Clinic II, University Heart Center Luebeck, Luebeck, Germany
2. DZHK (German Research Centre for Cardiovascular Research), Partner Site Hamburg/Lübeck/Kiel, 23562 Lübeck, Germany
Interests: immunology; cardiology; vascular biology

Special Issue Information

Dear Colleagues,

Platelets are remarkably versatile cells, widely recognized for their central role in primary hemostasis. Their significance as key targets for pharmacological therapy in both primary and secondary prevention, as well as after vascular interventions involving the implantation of exogenous materials into the bloodstream, is well established. Moreover, the involvement of platelets in atherosclerosis is undisputed.

Recently, platelets have also been implicated in various tissue remodeling processes, such as apoptosis, immune patrolling, and adaptive immunity. They play a critical role in the immediate response to vascular injury by promoting vascular inflammation and immunomodulation. These discoveries have led to a broader understanding of platelets as immune cells.

Platelets continue to captivate both clinicians and basic scientists as new interactions between platelets, their precursor cells (megakaryocytes), and novel immune cell populations are uncovered. Emerging roles of platelets in disease mechanisms are being identified, and they are increasingly recognized as valuable targets for therapeutic interventions and as potential biomarkers.

Contributions to this Special Issue, "Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential", should focus on recent advancements that reinforce the concept of platelets as crucial mediators of vascular immunity, integral components of the immune system, promising therapeutic targets, or biomarkers, particularly in relation to their lipidome, transcriptome, or proteome.

Dr. Henry Nording
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • platelet biology
  • vascular immunity
  • atherosclerosis
  • therapeutic targets
  • biomarkers

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

15 pages, 2993 KiB  
Article
Cold vs. Room Temperature: A Comparative Analysis of Platelet Functionality in Cold Storage
by Panagiotis V. Drossos, Sotirios P. Fortis, Alkmini T. Anastasiadi, Efthymia G. Pavlou, Andreas G. Tsantes, Gerasimos A. Spyratos, Effie G. Papageorgiou, Efrosyni G. Nomikou, Konstantinos E. Stamoulis, Georgios Dryllis, Vassilis L. Tzounakas, Marianna Politou, Serena Valsami and Anastasios G. Kriebardis
Biomedicines 2025, 13(2), 310; https://doi.org/10.3390/biomedicines13020310 - 27 Jan 2025
Viewed by 725
Abstract
Background: The platelet functionality of cold-stored platelets remains a subject of debate. Our aim was to investigate the effect of temperature on the hemostatic properties of stored platelets. Methods: Ten split pooled platelets stored at cold and at room temperature were evaluated in [...] Read more.
Background: The platelet functionality of cold-stored platelets remains a subject of debate. Our aim was to investigate the effect of temperature on the hemostatic properties of stored platelets. Methods: Ten split pooled platelets stored at cold and at room temperature were evaluated in vitro on storage days 1, 5, 10, and 15 for metabolic, physiological, and vesiculation parameters, as well as their hemostatic profile using rotational thromboelastometry (ROTEM®). Results: The integrity profile was better preserved in the cold-stored platelets, as lower lactate dehydrogenase levels were documented (e.g., day 10: 261 ± 46 vs. 572 ± 220 U/L, 4 vs. 22 °C, p = 0.004). A time-dependent decrease in hemostatic capacity was evident regardless of the temperature, but the cold-stored units were linked to shorter clot initiation times and increased elasticity, strength, and firmness parameters, especially during extended storage (e.g., maximum clot firmness, INTEM day 15: 81 ± 2 vs. 19 ± 4 mm, 4 vs. 22 °C, p = 0.0008). Additionally, the aggregation of cold-stored platelets was superior after the addition of any agonist tested. Regarding vesiculation parameters, the extracellular vesicles of the units at 4 °C were characterized by a larger size from day 10 onwards, when they also presented higher procoagulant activity (e.g., phospholipid-dependent clotting time of day 15: 21.4 ± 2.3 vs. 25.0 ± 3.0 s, 4 vs. 22 °C, p = 0.016). Conclusion: Our results indicate that cold-stored platelets perform better than those stored at room temperature, demonstrating superior clot formation and stability. This suggests that cold storage may more effectively preserve platelet function, potentially offering advantages for transfusion therapy and the extension of shelf-life. However, the clinical relevance of these findings requires further investigation. Full article
(This article belongs to the Special Issue Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential)
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Figure 1

Figure 1
<p>Metabolic, integrity, and activity parameters of cold-stored versus conventionally stored platelets (<span class="html-italic">n</span> = 10 per group). ROS: reactive oxygen species; LDH: lactate dehydrogenase; RT: room temperature; PPL: procoagulant phospholipid; PS: phosphatidylserine. (*) <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">Figure 2
<p>Vesiculation parameters of cold-stored versus conventionally stored platelets (<span class="html-italic">n</span> = 10 per group) using nanoparticle tracking analysis (NTA). RT: room temperature; EV: extracellular vesicles; PLT: platelet. (*) <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">Figure 3
<p>Assessment of the viscoelastic properties of the cold-stored versus conventionally stored platelets (<span class="html-italic">n</span> = 10 per group) after the addition of tissue factor (EXTEM assay). RT: room temperature; Ax: amplitude x minutes after clotting time (CT); ARx: area under the curve (AUC) from CT to x minutes. (*), numbers in bold: <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">Figure 4
<p>Assessment of the viscoelastic properties of the cold-stored versus conventionally stored platelets (<span class="html-italic">n</span> = 10 per group) after coagulation activation via the contact phase (INTEM assay). RT: room temperature; Ax: amplitude x minutes after clotting time (CT); ARx: area under the curve (AUC) from CT to x minutes. (*), numbers in bold: <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">Figure 5
<p>Aggregation of the cold-stored versus conventionally stored platelets (<span class="html-italic">n</span> = 10 per group) after induction by different agonists. The results on x-aris are in maximum percentage (max %) aggregation; RT: room temperature; ADP: adenosine diphosphate. (*) <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">
12 pages, 1321 KiB  
Article
TRAP-Induced Platelet Reactivity Is Inhibited by Omega-3 Fatty Acid-Derived Prostaglandin E3 (PGE3)
by José-Miguel Osete, Faustino García-Candel, Francisco-José Fernández-Gómez, Miguel Blanquer, Noemí M. Atucha, Joaquín García-Estañ and David Iyú
Biomedicines 2024, 12(12), 2855; https://doi.org/10.3390/biomedicines12122855 - 16 Dec 2024
Viewed by 774
Abstract
Background: Prostaglandins are naturally occurring local mediators that can participate in the modulation of the cardiovascular system through their interaction with Gs/Gi-coupled receptors in different tissues and cells, including platelets. Thrombin is one of the most important factors that regulates platelet reactivity and [...] Read more.
Background: Prostaglandins are naturally occurring local mediators that can participate in the modulation of the cardiovascular system through their interaction with Gs/Gi-coupled receptors in different tissues and cells, including platelets. Thrombin is one of the most important factors that regulates platelet reactivity and coagulation. Clinical trials have consistently shown that omega-3 fatty acid supplementation lowers the risk for cardiovascular mortality and morbidity. Since omega-3 fatty acids are the main precursors of PGE3 in vivo, it would be relevant to investigate the effects of PGE3 on Thrombin Receptor Activating Peptide (TRAP-6)-induced platelet reactivity to determine the receptors and possible mechanisms of action of these compounds. Methods: We have measured platelet aggregation, P-selectin expression, and vasodilator-stimulated phosphoprotein (VASP) phosphorylation to evaluate platelet reactivity induced by TRAP-6 to determine the effects of PGE3 on platelet function. Results: We assessed the ability of DG-041, a selective prostanoid EP3 receptor antagonist, and of ONO-AE3-208, a selective prostanoid EP4 receptor antagonist, to modify the effects of PGE3. PGE3 inhibited TRAP-6-induced platelet aggregation and activation. This inhibition was enhanced in the presence of a Gi-coupled EP3 receptor antagonist and abolished in the presence of a Gs-coupled EP4 receptor antagonist. The effects of PGE3 were directly related to changes in cAMP, assessed by VASP phosphorylation. Conclusions: The general effects of PGE3 on human platelet reactivity are the consequence of a balance between activatory and inhibitory effects at receptors that have contrary effects on adenylate cyclase. These results indicate a potential mechanism by which omega-3 fatty acids underlie cardioprotective effects. Full article
(This article belongs to the Special Issue Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential)
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Figure 1

Figure 1
<p>Effects of selective prostanoid receptor antagonists on the PGE3-mediated changes in TRAP-6-induced platelet aggregation. The effects of PGE3 in the absence and presence of the EP3 antagonist DG-041 (3 μM), and the EP4 antagonist ONO-AE3-208 (1 μM) on platelet aggregation induced by TRAP-6 (10 μM), over a 4 min period, in whole blood. Aggregation was determined by flow cytometry and measured by single platelet counting method. The results shown are the mean ± SEM of 6 experiments. *** <span class="html-italic">p</span> = 0.0004, **** <span class="html-italic">p</span> &lt; 0.0001.</p> Full article ">Figure 2
<p>Effects of selective prostanoid receptor antagonists on PGE3-mediated changes in TRAP-6-induced P-selectin expression. The effects of PGE3 in the absence and presence of the EP3 antagonist DG-041 (3 μM), and the EP4 antagonist ONO-AE3-208 (1 μM), on platelet P-selectin expression induced by TRAP-6 (10 μM), over a 4 minute period, in whole blood. P-selectin was measured by flow cytometry and is presented as median fluorescence (mf). The results shown are the mean ± SEM of 6 experiments. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.005.</p> Full article ">Figure 3
<p>Effects of selective prostanoid receptor antagonists on the PGE3 mediated changes in TRAP-6-induced VASP-phosphorylation. The effects of PGE3 in the absence and presence of the EP3 antagonist DG-041 (3 μM), and the EP4 antagonist ONO-AE3-208 (1 μM) on VASP phosphorylation, over a 4 min period, in whole blood. VASP-phosphorylation was determined by flow cytometry using a cytometric bead array (VASPFix) and is presented as median fluorescence (mf). The results shown are the mean ± SEM of 6 experiments. ** <span class="html-italic">p</span> &lt; 0.005, *** <span class="html-italic">p</span> = 0.0008, **** <span class="html-italic">p</span> &lt; 0.0001.</p> Full article ">Figure 4
<p>Diagrammatic view of the receptors and their consequent effects on adenylate cyclase, which mediates the effects of PG3 on platelet function (modified from Iyú D et al. [<a href="#B24-biomedicines-12-02855" class="html-bibr">24</a>]).</p> Full article ">
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