Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi in Psoriasis and Psoriatic Arthritis, 2017
Cell adhesion is an ancient and basic process of any living system. Even unicellular organisms interact with the extracellular environment (e.g., protozoa invading a host) using CAMs, in addition to receptors for soluble molecules. The term membrane receptor usually applies to a cell membrane molecule whose ligand is soluble, whereas when the ligand is large or insoluble or bound to another cell or matrix, then the receptor, and sometimes the ligand as well, may be considered a CAM, although the nomenclature is largely convention based. When the ligand is very similar to the receptor itself and located in another cell, it is called a homotypic adhesion molecule (e.g., cadherin), and when the ligand on the other cell is different, it is called heterotypic CAM. CAMs are involved in the development, differentiation, and function of all cells. We will focus on the role of adhesion molecules in inflammation and angiogenesis.
Integrin-Dependent Responses in Human Basophils
Bruce S. Bochner in Adhesion Molecules in Allergic Disease, 2020
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.
Tyrosine Phosphatases as New Treatment Targets in Acute Myeloid Leukemia
Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey in Innovative Leukemia and Lymphoma Therapy, 2019
The first category is the largest family and consists of the class I cysteine-based PTPs. The 38 strictly tyrosine-specific “classical PTPs” belong to this family and can be further divided into trans-membrane, receptor-like PTPs (RPTPs), and the intracellular, nonreceptor PTPs (NRPTPs) (15). The RPTPs have a single trans-membrane and variable extracellular domain. The intracellular parts of most of the RPTPs contain two tandem PTP domains, D1 and D2, with most of the catalytic activity resident in D1. In many cases, the extracellular domains include immunoglobulin like and fibronectin type III domains. These domains are similar to the extracellular domains of cellular adhesion molecules (16). NRPTPs have striking structural diversity and often contain sequences that target them to specific subcellular locations or enable their binding to specific proteins (17). The 61 dual specificity phosphatases (DSPs), or VH-1 like enzymes, also belong to the class I cysteine-based PTPs. DSPs are able to dephosphorylate serine and threonine residues in their protein substrates in addition to tyrosine residues. This group can be further divided into seven subgroups. MKPs are specific for the mitogen-activated protein kinases (MAPKs) (18,19); atypical DSPs (20) include 19 poorly characterized enzymes; phosphatase and tensin homologs (PTENs) and myotubularins dephosphorylate the D3-phosphate of inositol phospholipids (21); PRLs and slingshots are poorly understood; and CDC14s are involved in dephosphorylating cyclin-dependent kinases (Cdks) and exit mitosis (22).
The effect of adalimumab on the vasculature in psoriatic skin lesions
Published in Journal of Dermatological Treatment, 2019
S. C. A. Hanssen, C. J. M. van der Vleuten, P. E. J. van Erp, M. M. B. Seyger, P. C. M. van de Kerkhof
Adalimumab modulates biological processes induced or regulated by TNF-α, including changes of expression of adhesion molecules. Adhesion molecules, proteins located on the cell surface, are involved in binding with other cells or with the extracellular matrix. Adhesion molecules play a key role in the recruitment and migration of immune cells such as leukocytes; it is presumed that adhesion molecules also play a crucial role in the regulation of neovascularization and formation of atherosclerosis (4). Various authors investigated the mechanism of action of TNF-α inhibitors in psoriatic patients, focusing on different features of the pathogenesis of psoriasis, such as immune responses and keratinocyte differentiation. Although, TNF-α also has effects on the endothelium, these effects of anti-TNF-α treatment on the (micro) vasculature in psoriasis have not been studied before.
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).
Related Knowledge Centers
- Antibody
- Cadherin
- Cytoskeleton
- Integrin
- Proteoglycan
- Extracellular Matrix
- Cell Surface Receptor
- Molecular Binding
- Membranome Database
- Immunoglobulin Superfamily