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Dear Colleagues,

Circulating platelets are highly reactive cell types that respond to a myriad of environmental cues to form homotypic aggregates as well as heterotypic interactions with leukocytes and endothelia. These events not only support a spectrum of normal homeostatic processes such as blood vessel integrity, initiation of the coagulation cascade, and immunological responses, but also ischemic pathologies and coagulopathies. Signaling events within platelets are well understood, but new inputs and modulators are being identified that provide insight as to how platelets produce unique responses in vivo.

This Special Issue of the International Journal of Molecular Sciences, entitled “Platelet Signaling and Coagulation”, will emphasize signaling pathways leading to critical platelet functions in hemostasis, coagulopathy, and thrombosis. The goal is to provide a broad view of platelet reactivity at the molecular level in a variety of physiological contexts. We invite you to contribute original research or focused reviews on the above topics for this Special Issue. We particularly welcome submissions from postdocs, PhD students, and young researchers.

We look forward to reading about your insights and exciting discoveries that further advance our knowledge of this crucial cell type in health and disease.

Dr. Stephen P. Holly
Dr. Rinku Majumder
Guest Editors

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Keywords

platelet
signaling
coagulation
aggregation
thrombosis
hemostasis
protein S
COVID-19

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Review

11 pages, 812 KiB

Open AccessReview

Systemic Review of Clot Retraction Modulators

by Alaina Guilbeau and Rinku Majumder

Int. J. Mol. Sci. 2023, 24(13), 10602; https://doi.org/10.3390/ijms241310602 - 25 Jun 2023

Viewed by 1666

Abstract

Through a process termed clot retraction, platelets cause thrombi to shrink and become more stable. After platelets are activated via inside-out signaling, glycoprotein αIIbβIII binds to fibrinogen and initiates a cascade of intracellular signaling that ends in actin remodeling, which causes the platelet to change its shape. Clot retraction is also important for wound healing. Although the detailed molecular biology of clot retraction is only partially understood, various substances and physiological conditions modulate clot retraction. In this review, we describe some of the current literature pertaining to clot retraction modulators. In addition, we discuss compounds from Cudrania trucuspidata, Arctium lappa, and Panax ginseng that diminish clot retraction and have numerous other health benefits. Caffeic acid and diindolylmethane, both common in plants and vegetables, likewise reduce clot retraction, as do all-trans retinoic acid (a vitamin A derivative), two MAP4K inhibitors, and the chemotherapeutic drug Dasatinib. Conversely, the endogenous anticoagulant Protein S (PS) and the matricellular protein secreted modular calcium-binding protein 1 (SMOC1) both enhance clot retraction. Most studies aiming to identify mechanisms of clot retraction modulators have focused on the increased phosphorylation of vasodilator-stimulated phosphoprotein and inositol 1,4,5-triphosphate receptor I and the decreased phosphorylation of various phospholipases (e.g., phospholipase A2 (PLA₂) and phosphatidylinositol-specific phospholipase Cγ2 (PLCγ₂), c-Jun N-terminal kinase, and (PI3Ks). One study focused on the decreased phosphorylation of Sarcoma Family Kinases (SFK), and others have focused on increased cAMP levels and the downregulation of inflammatory markers such as thromboxanes, including thromboxane A2 (TXA₂) and thromboxane B2 (TXB₂); prostaglandin A2 (PGE2); reactive oxygen species (ROS); and cyclooxygenase (COX) enzyme activity. Additionally, pregnancy, fibrinolysis, and the autoimmune condition systemic lupus erythematosus all seem to affect, or at least have some relation with, clot retraction. All the clot retraction modulators need in-depth study to explain these effects. Full article

(This article belongs to the Special Issue Platelet Signaling and Coagulation)

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