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Skin Morphology, Development and Physiology
Published in Heather A.E. Benson, Michael S. Roberts, Vânia Rodrigues Leite-Silva, Kenneth A. Walters, Cosmetic Formulation, 2019
Kenneth A. Walters, Michael S. Roberts
In addition to hemidesmosome cell-matrix binding, another site for adhesion of the cells of the epidermal basal layer and the basal membrane is the adherens junction (Kaiser et al., 1993; Niessen, 2007), in which there are two basic adhesive units. Nectins are IgG-like adhesion receptors that possess a transmembrane region and form an adhesive unit with the actin-binding protein, afadin. In addition to this unit, cadherins are transmembrane proteins that link to α-, β- and p120 catenins. Adherens junctions appear more frequently in the upper epidermis (Ishiko et al., 2003).
Structure and function of skin
Published in Roger L. McMullen, Antioxidants and the Skin, 2018
Another type of cell junction that provides a strong mechanical linkage between cells are adherens junctions. There are two types of adherens junctions, which differ in their protein structure and organization. One adherens structure is the cadherin-catenin complex, the other a nectin-afadin complex. Both complexes are anchored to keratinocytes by actin filaments located in the cytoplasm of the cell. Overall, adherens junctions provide another form of cellular connectivity, thereby providing mechanical strength for tissue organization.11
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
Cadherins are a family of ionic calcium-dependent CAMs with more than 100 members. Almost all cadherins are single-pass transmembrane glycoproteins with repetitive extracellular β-sandwich extracellular cadherin domains that adopt a similar fold to Ig domains. There are only a few exceptions, for example, (1) nonclassical member invertebrate flamingo/starry-night and its vertebrate homolog Celsr1,2,3 (cadherin, EGF laminin-G seven-pass G-type receptor 1), which are seven-transmembrane GPCRs with the N-terminus like a cadherin, and (2) T-cadherin, which instead of a transmembrane tail has a gpI anchor. Large organized clusters of cadherin zip up along zones across the cell membrane, leading to various forms of cell–cell junctions, like zonula adherens (or adherens junctions), for example, in epithelial cells, macula adherens (desmosome), and in keratinocytes, fascia adherens (e.g., part of the intercalated disc in cardiomyocytes).
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
Arrived CTCs undergo extravasation (the opposite process of intravasation) to establish metastasis. Extravasation involves different steps: rolling, firm adhesion, and finally, trans-endothelial migration (TEM) (luminal to the abluminal faces of the endothelium) for crossing blood-brain barriers. BCCs slowly roll along brain microvascular endothelial cells (BMVECs) surface to establish various receptor-ligand interactions with endothelial cells (ECs) [60,62]. Once the interaction is established at a suitable site of the blood-brain barrier (BBB), firm and stable adhesion between BCCs and EC takes place. E-selectin plays an important role in this step [63]. Tumor cells release VEGF to facilitate the TEM through the endothelial barrier [55,64]. TEM mostly takes place in paracellular pathways. The involvement of the transcellular pathway in the extravasation process is unclear. Tumor cells interact first with tight junctions and then with adherens junctions to allow paracellular TEM. The absence of detectable BMVECs programmed cell death or any significant disruptive changes at TEM sites suggests that transmigration of tumor cells does not lead to BBB damage [65]. Additionally, similar to the EMT of epithelial cells, ECs may undergo an endothelial-mesenchymal transition (EndMT) [66]. Anderberg et al. [67] suggested that EndMT occurs in extravasation and intravasation. This process allows the endothelial cell to acquire a mesenchymal phenotype to weaken the endothelial barrier [67]. Thus, EndMT facilitates extravasation. As such, extravasation is a potential area of therapeutic development.
Critical roles of adherens junctions in diseases of the oral mucosa
Published in Tissue Barriers, 2023
Christina Kingsley, Antonis Kourtidis
Adherens junctions (AJs) are fundamental cell–cell adhesion structures, typically located at apical areas of cell–cell contact in polarized differentiated epithelia, between tight junctions (TJs), which lie more apically, and desmosomes, found more basolaterally.18,22,23 The intimate crosstalk of the AJs with the TJs is essential for formation of the epithelial barrier.24–26 In stratified epithelial tissues, such as those lining the oral mucosa, TJs are exclusively present at the stratum granulosum, where the barrier is eventually established.2,13,18,22,27 Nevertheless, AJs, as well as desmosomes, are also interspersed throughout areas of cell–cell contact in the underlying layers of the stratified epithelium, where they play critical roles for tissue organization, tissue stratification, and mechanical stability.18,22,23 Overall, AJs are abundant throughout most of the oral mucosal epithelium, as well as the gingival epithelium and sulcular epithelium. Relatively fewer AJs, as well as fewer desmosomes, are found in the junctional epithelium, since increased permeability and wide intercellular spaces are desired there to allow passage of immune cells, such as neutrophils and leucocytes that protect the periodontal area from pathogens.2,6,8
Epithelial integrity, junctional complexes, and biomarkers associated with intestinal functions
Published in Tissue Barriers, 2022
Arash Alizadeh, Peyman Akbari, Johan Garssen, Johanna Fink-Gremmels, Saskia Braber
The lining epithelial cells are connected by multiple protein structures denoted as apical junctional complexes, including tight junctions (TJs), adherens junctions, and desmosomes (Figure 1).13–15 Adherens junctions play a role in initiation and stabilization of cell-cell contacts through a family of intercellular adhesion molecules and consist of transmembrane proteins, including E-cadherin and nectin as well as associated cytoplasmic proteins catenins, which are directly connected to the actin cytoskeleton.16 Desmosomes are patch-like intercellular junctions at the lateral sides of plasma membranes that join adjacent cells together and provide anchoring sites for intermediate filaments.15,17,18 TJ proteins are thought to be the most essential components of these multiple structures and it is now well-established that the mucosal barrier function cannot be maintained without a well-organized pattern of this anastomosing network of sealing strands comprising over 50 proteins. The intercellular space completely disappears at the level of TJs, whereas in adherens junctions and desmosomes, the adjacent membranes are 15–20 nm apart (Figure 1).13,16,17,19,20 Each individual component of the TJ network is structurally and functionally different, but closely interacts with each other to form an efficient and functional barrier.