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Biomolecules
Special Issues
New Discoveries in Biological Functions of Platelet
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New Discoveries in Biological Functions of Platelet

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 4625

Special Issue Editors

Dr. Attila Braun

E-Mail Website1 Website2
Guest Editor
Walther-Straub-Institute for Pharmacology and Toxicology, Ludwig-Maximilian-University, 80336 Munich, Germany
Interests: platelet signaling; ion homeostasis; channelopathies; SOCE; megakaryopoiesis
Dr. Elmina Mammadova-Bach

E-Mail Website1 Website2
Guest Editor
Walther-Straub-Institute for Pharmacology and Toxicology, Ludwig-Maximilian-University, 80336 Munich, Germany
Interests: tumor microenvironment; circulating blood cells; platelets; cancer-associated thrombosis; inflammatory ecosystem of tumors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Platelets are small, disc-shaped blood cells that play a vital role in hemostasis, or the prevention of bleeding after vessel injury. Although platelets have long been known to be involved in thrombosis, recent research has revealed new biological functions of these cells in other pathological complications, such as sepsis, diabetes, fibrosis, myocardial infarction, vasculitis, and cancer metastasis. Platelets have been found to interact with immune cells, such as neutrophils, monocytes, and lymphocytes, and modulate their effector functions. They can directly recognize and respond to bacterial and viral pathogens and release antimicrobial peptides and cytokines, which can help fight infections. Platelets can also interact with endothelial cells, leukocytes, and other inflammatory cells, releasing inflammatory mediators, such as thromboxane A2 (TXA2), prostaglandin E2 (PGE2), and interleukin-1 beta (IL-1β). These mediators can recruit and activate immune cells, promote vasodilation and vascular permeability, and enhance the production of cytokines and chemokines. In sepsis or virus infection, activated platelets promote extracellular trap formation and intravascular coagulation. Moreover, platelets contain growth factors, such as platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF), which promote tissue healing and regeneration. These growth factors can stimulate the proliferation and migration of endothelial cells, thereby supporting angiogenesis. Finally, platelets have been found to play a role in different steps of tumor progression. They directly interact with cancer cells, promoting their survival and transmigration through the endothelium, leading to tumor metastasis. Platelets contribute to the formation of the pre-metastatic niche by promoting the recruitment and activation of immune cells and by releasing cytokines and growth factors that support angiogenesis and tumor cell survival. Additionally, platelets can modulate the response of cancer cells to immunotherapy and chemotherapy, promoting tumor cell survival and resistance to these treatments. Recent research has revealed important insights into the complex interplay between platelets, immune and cancer cells, leading to new discoveries of platelets in cancer-associated thrombosis and thrombo-inflammation.

Our open-access journal, Biomolecules, is currently hosting an important Special Issue entitled “New Discoveries in the Biological Functions of Platelets”, including the indicated topics. The submission deadline for this Special Issue is 1 October 2023. You are welcome to submit your manuscript now or at any point up until the deadline.

Dr. Attila Braun
Dr. Elmina Mammadova-Bach
Guest Editors

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. Biomolecules 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 2700 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

  • platelets
  • thrombosis
  • sepsis
  • coagulopathy
  • blood clotting
  • diabetes
  • vascular integrity/permeability
  • wound healing
  • tissue regeneration
  • fibrosis
  • vasculitis
  • immune cells
  • inflammation
  • extracellular traps
  • angiogenesis
  • tumor growth and metastasis
  • anti-platelet and anti-thrombotic therapies

Published Papers (2 papers)

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Research

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15 pages, 2728 KiB  
Article
Mind the Gap: Model-Based Switching from Selatogrel to Maintenance Therapy with Oral P2Y12 Receptor Antagonists
by Chih-hsuan Hsin, Jasper Dingemanse, Andrea Henrich, Corine Bernaud, Martine Gehin and Andreas Krause
Biomolecules 2023, 13(9), 1365; https://doi.org/10.3390/biom13091365 - 08 Sep 2023
Cited by 1 | Viewed by 991
Abstract
Background: The P2Y12 receptor antagonist selatogrel is being developed for subcutaneous self-administration with a ready-to-use autoinjector at the onset of acute myocardial infarction (AMI) symptoms. The unique pharmacological profile of selatogrel (fast, potent, and short-acting) can bridge the time gap between the [...] Read more.
Background: The P2Y12 receptor antagonist selatogrel is being developed for subcutaneous self-administration with a ready-to-use autoinjector at the onset of acute myocardial infarction (AMI) symptoms. The unique pharmacological profile of selatogrel (fast, potent, and short-acting) can bridge the time gap between the onset of AMI and first medical care. A clinical Phase 1 study showed a time-dependent pharmacodynamic interaction between selatogrel and loading doses of clopidogrel and prasugrel. As treatment switching is a common clinical practice, the assessment of subsequent switching from a clopidogrel loading dose to the first maintenance dose of oral P2Y12 receptor antagonists is highly relevant. Objectives: Model-based predictions of inhibition of platelet aggregation (IPA) for the drugs triggering pharmacodynamic interactions were to be derived to support clinical guidance on the transition from selatogrel to oral P2Y12 receptor antagonists. Methods: Scenarios with selatogrel 16 mg administration or placebo followed by a clopidogrel loading dose and, in turn, prasugrel or ticagrelor maintenance doses at different times of administration were studied. Population pharmacokinetic/pharmacodynamic modeling and simulations of different treatment scenarios were used to derive quantitative estimates for IPA over time. Results: Following selatogrel/placebo and a clopidogrel loading dose, maintenance treatment with ticagrelor or a prasugrel loading dose followed by maintenance treatment quickly achieved sustained IPA levels above 80%. Prior to maintenance treatment, a short time span from 18 to 24 h was identified where IPA levels were predicted to be lower with selatogrel than with placebo if clopidogrel was administered 12 h after selatogrel or placebo. Predicted IPA levels reached with placebo alone and a clopidogrel loading dose at 4 h were consistently lower than with selatogrel administration, followed by a clopidogrel loading dose at 12 h. If a clopidogrel loading dose is administered at 12 h, selatogrel maintains higher IPA levels up to 16 h. IPA levels are subsequently lower than on the placebo until the administration of the first maintenance dose. Conclusions: Model-based predictions informed the transition from selatogrel subcutaneous administration to oral P2Y12 therapy. The application of modeling techniques illustrates the value of employing pharmacokinetic and pharmacodynamic modeling for the simulation of various clinical scenarios of switching therapies. Full article
(This article belongs to the Special Issue New Discoveries in Biological Functions of Platelet)
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Review

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20 pages, 1164 KiB  
Review
Platelet and HIV Interactions and Their Contribution to Non-AIDS Comorbidities
by Thomas Awamura, Elizabeth S. Nakasone, Louie Mar Gangcuangco, Natalie T. Subia, Aeron-Justin Bali, Dominic C. Chow, Cecilia M. Shikuma and Juwon Park
Biomolecules 2023, 13(11), 1608; https://doi.org/10.3390/biom13111608 - 02 Nov 2023
Viewed by 3126
Abstract
Platelets are anucleate cytoplasmic cell fragments that circulate in the blood, where they are involved in regulating hemostasis. Beyond their normal physiologic role, platelets have emerged as versatile effectors of immune response. During an infection, cell surface receptors enable platelets to recognize viruses, [...] Read more.
Platelets are anucleate cytoplasmic cell fragments that circulate in the blood, where they are involved in regulating hemostasis. Beyond their normal physiologic role, platelets have emerged as versatile effectors of immune response. During an infection, cell surface receptors enable platelets to recognize viruses, resulting in their activation. Activated platelets release biologically active molecules that further trigger host immune responses to protect the body against infection. Their impact on the immune response is also associated with the recruitment of circulating leukocytes to the site of infection. They can also aggregate with leukocytes, including lymphocytes, monocytes, and neutrophils, to immobilize pathogens and prevent viral dissemination. Despite their host protective role, platelets have also been shown to be associated with various pathophysiological processes. In this review, we will summarize platelet and HIV interactions during infection. We will also highlight and discuss platelet and platelet-derived mediators, how they interact with immune cells, and the multifaceted responsibilities of platelets in HIV infection. Furthermore, we will give an overview of non-AIDS comorbidities linked to platelet dysfunction and the impact of antiretroviral therapy on platelet function. Full article
(This article belongs to the Special Issue New Discoveries in Biological Functions of Platelet)
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