Phospholipids and the Clotting Process
E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson in Phospholipid-Binding Antibodies, 2020
In most if not all cells, lipid asymmetry is maintained during the lifetime of the cell. Apparently, platelets are no exception to this rule unless they become activated. Two regulatory mechanisms have been proposed for the maintenance of phospholipid asymmetry in biological membranes, and it seems likely that loss of membrane lipid asymmetry involves alterations in these regulatory systems. The two mechanisms which are usually considered are (1) binding of amino-phospholipids to cytoskeletal proteins at the cytoplasmic surface of the membrane,103-106 and (2) pumping of amino-phospholipids from the outside to the inside of the cell membrane by an ATP-dependent lipid flip-flop catalyst in the membrane, usually referred to as amino-phospholipid translocase.106-110 Alterations in these mechanisms may occur during platelet activation as will be discussed below.
The Etiology of the Antiphospholipid Syndrome
Howard J.A. Carp in Recurrent Pregnancy Loss, 2020
Other mechanisms may be responsible for thrombogenesis. aPT antibodies may induce TF expression and improve the binding between prothrombin (PT) and the surface of endothelial cells, leading to thrombogenesis. Other studies have shown that thrombotic activity is related to the presence of antiphosphatidylserine-prothrombin complex (aPS/PT), rather than aPT itself. This complex is more frequently found in patients with lupus anticoagulant (LA), but its association with thrombosis seems to be independent of the presence of LA [26]. APT might also bind thrombin, preventing its inactivation by antithrombin (AT) [27]. Thrombin activation can lead to platelet activation. Tissue factor−related procoagulant activity and tissue factor mRNA levels in monocytes are increased in PAPS with thrombosis when compared to those without thrombosis.
The Immune System and its Function
Istvan Berczi in Pituitary Function and Immunity, 2019
The principal role of the platelet is related to blood coagulation. Platelets adhere specifically to several substances such as collagen; they may aggregate and/or undergo a secretory response called the release reaction.29 It is clear, however, that platelet aggregation and release can be triggered immunologically by immune complexes, activated complement components, and also by lymphokines. Thus, it is not surprising that platelets were shown to have a role in systemic anaphylaxis30,31 and in graft rejection.32 Moreover, mouse platelets were shown to lyse antibody-coated erythrocytes, but nucleated cells were unaffected. Most classes of mouse immunoglobulins can initiate the platelet-mediated lytic reaction.33 The IgE mediated killing of schistosomes by human and rat platelets has also been observed recently.23 Taking into consideration that platelets represent 34% of the leukocyte volume they may indeed exert a massive defense mechanism against parasites. Similarly, thrombocytes, which are three times more abundant than other circulating phagocytes, were identified as the primary circulating phagocytic cells in chickens.34
Orally delivered rutin in lipid-based nano-formulation exerts strong antithrombotic effects by protein disulfide isomerase inhibition
Published in Drug Delivery, 2022
Dan Chen, Yurong Liu, Peiwen Liu, Yang Zhou, Longguang Jiang, Cai Yuan, Mingdong Huang
Thrombosis, the occlusion of blood vessels by localized clots, can occur in both macrocirculation and microcirculation, and becomes the central pathological event in various vascular diseases, including myocardial infarction, stroke, and pulmonary embolism (Mackman, 2008; Wendelboe & Raskob, 2016). During clot formation, the recruitment of activated platelets occurs in parallel with the blood coagulation cascade. Both processes communicate and promote each other to generate glue-like fibrin to seal the injured vessel. Currently, antiplatelets and anticoagulants are a mainstay for thrombosis prevention. However, there is an inherent risk of bleeding for these agents, which results in adverse cardiovascular events and negates the potential clinical benefit (Mackman, 2008; Melnikova, 2009; Lin et al., 2015b). Therefore, there are extensive and continuous efforts to develop novel antithrombotics with favorable potency and safety.
Inhibition of platelet activation using vitamins
Published in Platelets, 2020
Gennadi Kobzar
Activated platelets participate in the blood clotting process by forming platelet aggregates and are involved in the development of atherosclerosis[1, 2] A number of compounds produced by blood cells and the vessel wall regulate platelet activation promoting platelet activation and aggregation or inhibiting this process. Anti-platelet therapy is widely used in the treatment of thrombosis. There is increasing evidence that some fruits, vegetables and spices have a beneficial effect on platelet function[3]. Regular consumption of fruits might be a convenient and effective mean for the prevention of vascular diseases. The extracts of many fruits and vegetables have been shown to have anti-platelet properties[4]. Some vitamins that inhibited platelet aggregation were found in these extracts. Vitamins can inhibit platelets through different mechanisms. The effective concentrations of vitamins in vitro are much higher than those found in circulating blood after their supplementation. Nevertheless, many epidemiological data and studies with supplementation have suggested the effectiveness of vitamins on platelets.
Swimming improves platelet dysfunction in mice fed with a high-fat diet
Published in Archives of Physiology and Biochemistry, 2023
Xinyong Su, Xiao Yu, Ruzhuan Chen, Weihua Bian
Platelets are an important component of mammalian blood and are small pieces of cytoplasm derived from mature megakaryocytes (Fu et al.2019). They can not only participate in normal physiological hemostasis but also play an important role in immunity and tissue repair (Rayes et al. 2019). Excessive aggregation of platelets will occur when their reactivity is increased, leading to the formation of a thrombus (Salamah et al.2018, Cardenas et al.2019). Platelet activation is related to a variety of intracellular signalling pathways. The level of pAKT, the activated form of AKT, increases when the platelet is activated (Li et al.2019). pAKT can promote the formation of platelet pseudopodia, the adhesion and spread of platelets, the release of α-granules and adenosine triphosphate in dense granules, and the binding of fibrinogen with the αIIb/β3 receptor on the surface of platelets. Inhibiting pAKT activity can inhibit the activation of the αIIb/β3 receptor, thereby inhibiting platelet reactivity (Chen et al.2004, Kwon, 2019).
Related Knowledge Centers
- Cell Adhesion
- Fibrin
- Hemostasis
- Endothelium
- Platelet
- Thrombus
- Blood
- Gel
- Platelet-Activating Factor
- Tissue Factor