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Haemostasis and Thrombosis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Vascular spasm (vasoconstriction) and the endotheliumVasoconstrictionA brief intense contraction of blood vessels.Decreases blood flow to the area of injury.In response to vascular injury or inflammation, the endothelium becomes prothrombotic.It downregulates the expression of anti-thrombotic molecules.It expresses procoagulant tissue factor (TF).It expresses adhesion molecules which mediate platelet and leucocyte capture.It releases the von Willebrand factor (VWF) which mediates platelet capture and aggregation.It releases plasminogen activator inhibitor-1 (PAI-1: inhibits fibrinolysis).
Integrin-Dependent Responses in Human Basophils
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Jane A. Warner, Kirsty Rich, Kirstin Goldring
In addition to their ability to regulate adhesion and migration, a substantial body of evidence has accumulated to suggest that adhesion molecules fulfill a much wider spectrum of roles. Interactions of the selectins or β2 integrins with their counter-ligands may cause conformational changes in the other adhesion proteins (22–25), facilitating firm adhesion to the endothelial surface. However, L-selectin is rapidly shed from the cell surface by proteolytic cleavage (26,27), and the function of β2 integrins are also down-regulated within a relatively short time frame (28,29), suggesting that their effects on cell function are likely to be short lived. This leaves the β1 integrins, which modulate firm adhesion to VCAM-1 and act as receptors for the extracellular matrix relaying signals from the external environment into the cell interior. These signals allow the cell to respond to its environment and modulate its responses accordingly; they have been shown to regulate many different aspects of cell function, including growth, differentiation, receptor expression, gene expression, and cell movement (30–34). Much of our knowledge of basophil integrins is derived from models developed in closely related cells; thus, it is relevant to summarize some of the effects of integrin ligation in mast cells and eosinophils.
Cell structure, function and adaptation
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Cells are joined by several types of cell junction that are physical connections. Desmosomes and tight junctions join cell membranes, and gap junctions allow passage of chemical messages between cells. In addition, adhesion molecules are expressed on cell surfaces, not only joining cells together but also transducing signals important for growth, migration, and differentiation. The surface-bound major histocompatibility complex (MHC) molecules and immunoglobulin are specialized forms of recognition mechanism present in lymphocytes, without which an immune response would be impossible.
Pathology of breast cancer metastasis and a view of metastasis to the brain
Published in International Journal of Neuroscience, 2023
Md Sakibuzzaman, Shahriar Mahmud, Tanzina Afroze, Sawsan Fathma, Ummul Barakat Zakia, Sabrina Afroz, Farzina Zafar, Maksuda Hossain, Amit Barua, Sabiha Akter, Hasanul Islam Chowdhury, Eram Ahsan, Shayet Hossain Eshan, Tasnuva Tarannum Fariza
The first step of metastasis is CD from the primary breast tumor. EMT allows the epithelial cells to lose cell polarity along with cell-cell adhesion and to differentiate into mesenchymal cells acquiring an increased ability to migrate, invade, and evade apoptosis [3,36–38]. However, EMT is not mandatory for breast cancer metastasis to all sites [35]. Cell adhesion molecules (CAMs) mainly consist of epithelial proteins (cadherin, selectin, and integrin). Among them, E-cadherin plays a vital role in epithelial cell adhesion [39]. Loss of E-cadherin facilitates CD. CD induces the expression of mesenchymal proteins (N-cadherin and vimentin), downregulates the expression of E-cadherin [40,41], and stimulates resistance to programmed cell death [41,42]. Thus, BCCs acquire a mesenchymal phenotype in the process of EMT. The Wnt signaling pathway regulates EMT. The knockdown of lncRNA UCA1 increases the expression of a crucial CAM, decreases the expression of mesenchymal proteins, and demotes the Wnt signaling pathway required for EMT [43]. Therefore, lncRNA UCA1 could be a therapeutic target to suppress EMT.
Association of E-Selectin gene polymorphisms and serum E-Selectin level with risk of coronary artery disease in lur population of Iran
Published in Archives of Physiology and Biochemistry, 2023
Mobin Khoshbin, Seyyed Amir Yasin Ahmadi, Mostafa Cheraghi, Negar Nouryazdan, Mehdi Birjandi, Gholamreza Shahsavari
CAD affects both men and women. The risk factors are common among men and women, however, smoking has more effect on women (Yahagi et al.2015). Aetiology wise, atherosclerosis is an inflammatory process in which reactive oxygen species (ROS) are created by immune cells, endothelium, and smooth muscles. ROS participates in formation of thrombosis as well as affecting lipoproteins. In addition, ROS participates in changing bioavailability of nitric oxide (NO) (Gray et al.2016, Incalza et al.2018, Yalameha 2019). Therefore, CAD and ACS have multifactorial aetiology. From the viewpoint of the inflammatory basis of atherosclerosis, expression of adhesion molecules by endothelial cells results in adhesion and implantation of circulating immune cells especially monocytes in the region of atherosclerosis (Reiss and Glass 2006, Vigetti et al.2010). These adhesion molecules are inter-cellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-selectin and P-selectin (Demerath et al.2001). Nowadays the role of circulating levels of such molecules in susceptibility to atherosclerosis are investigated (Eikendal et al.2018). E-selectin results in adhesion of monocytes to endothelium and causes inflammation (Silva et al.2017).
Intravenous abciximab as a rescue therapy for immediate reocclusion after successful mechanical thrombectomy in acute ischemic stroke patients
Published in Platelets, 2022
François Delvoye, Stephane Loyau, Julien Labreuche, Guillaume Taylor, Benjamin Maier, Michel Piotin, Raphael Blanc, Simon Escalard, Lucas Di Meglio, Malek Ben Maacha, Hocine Redjem, Stanislas Smajda, Gabriele Ciccio, Solène Hébert, Candice Sabben, Martine Jandrot-Perrus, Alain Maertens De Noordhout, Mikael Mazighi, Benoit Ho-Tin-Noé, Jean-Philippe Desilles
In a previous study, we investigated the impact of intravenous thrombolytic treatment with tPA on platelet aggregation. We showed that tPA treatment could limit ATP-induced platelet aggregation, an effect due at least in part to the degradation of fibrin(ogen) [16]. Interestingly, although tPA can reduce platelet aggregation through fibrinogen degradation in platelet-rich plasma (PRP), we show here that this effect is not sufficient to prevent thrombosis in chamber experiments where thrombin formation is allowed in flowing whole blood. These observations raise the question of how and through which adhesion molecules platelets are recruited to the growing thrombus in this setting. The impact of abciximab suggests a substrate interacting with GPIIb/IIIa. Since abciximab not only blocks the interaction of GPIIb/IIIa with fibrin(ogen) but also with von Willebrand factor and fibronectin [17], it might be of interest to investigate the putative role of those adhesive molecules in mediating fibrin(ogen)-independent recruitment of platelets onto tissue factor/collagen surfaces in future studies.