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Tissue injury and repair
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Another important component of the extracellular matrix is a heterogeneous group of negatively charged polysaccharide chains known as glycosaminoglycans. The most abundant of these are hyaluronic acid, chondroitin sulphate, dermatan sulphate, and heparan sulphate. Except for hyaluronic acid, all the compounds are linked to a core protein to form proteoglycans. These are long unbranched structures, which form a water-replete gel. Proteoglycans may also be found within cell membranes (e.g. syndecan).
Pathogenesis
Published in Aparna Palit, Arun C. Inamadar, Systemic Sclerosis, 2019
The process of angiogenesis is mainly regulated by VEGF. It stimulates the migration and proliferation of ECs, increases vascular permeability, and induces tube formation. In SSc, VEGF is strongly expressed in skin and its serum level is also significantly increased. The latter bears significant correlation with fingertip ulceration in patients with SSc. Even though the VEGF levels are increased in SSc, the time kinetics of its expression plays a critical role in angiogenesis. The new vessels become untenable if upregulation of VEGF is transient. A prolonged overexpression results in uncontrolled fusion of new vessels resembling disturbed capillary network.10 Higher levels of syndecan-1 that binds to VEGF and presents them to respective receptors on endothelial cells has been demonstrated in SSc. Higher levels of syndecan-1 correlate with SSc vasculopathy, such as telangiectasia and PAH.11
Immunohistochemical Characterization of Extracellular Matrix in Tumor Tissues
Published in Róza Ádány, Tumor Matrix Biology, 2017
Syndecan, cell surface heparan sulfate proteoglycan, can bind to collagens and fibronectin through its heparan sulfate chains and mediate cell adhesion.18 Moreover, human syndecan binds to type I collagen and fibronectin, but not to laminin or vitronectin.19 Syndecan isolated from embryonic tooth mesenchyme can also bind tenascin via its heparan sulfate chains.20
Inflammatory markers calprotectin, NETs, syndecan-1 and neopterin in COVID-19 convalescent blood donors
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Geir Hetland, Magne Kristoffer Fagerhol, Veselka Petrova Dimova-Svetoslavova, Mohammad Reza Mirlashari, Nhan Trung Nguyen, Andreas Lind, Svein Olav Kolset, Arne Vasli Lund Søraas, Lise Sofie Haug Nissen-Meyer
Syndecans represent a family of cell surface proteoglycans carrying covalently attached glycosaminoglycan chains of the heparan sulphate or chondroitin sulphate type in the extracellular domain of the protein. The protein part is transmembrane and the cytosolic part is actively engaged in signal transduction [17]. There are five different syndecans, syndecan 1–5, with differences in cell and tissue distribution. The different domains of syndecans contribute to their functions as links between the extracellular and intracellular environment and their dynamic involvement in normal and pathological conditions. Shedding of syndecans has been linked to several types of diseases [18,19]. Recently, shedding of syndecan-1 has also been studied in relation to the severity of COVID-19 complications [20].
Epithelial damage in the cystic fibrosis lung: the role of host and microbial factors
Published in Expert Review of Respiratory Medicine, 2022
Arlene M. A. Glasgow, Catherine M. Greene
MMP-7 (or matrilysin) regulates the neutrophil chemotactic gradient during lung injury via cleavage of syndecan-1 from the epithelial cell surface, which releases CXCL1 [122]. It is also critical to the repair response, as MMP-7 inhibition impairs post-injury re-epithelialisation [123]. MMP-7 mediated syndecan-1 shedding facilitates cell migration and wound closure through its effects on alpha(2)beta(1) integrin activation [124]. MMP-10 (or stromelysin) appears to control inflammation during pathogenic colonization of bacteria via modulation of macrophage phenotype [125]. MMP-7 and MMP-10 are increased in the CF airway epithelium and alveolar macrophages, respectively [123,125]. Whilst it is clear that many MMPs contribute to the co-ordination of initiation and termination of the host immune response as well as roles in injury repair, more studies are needed to pinpoint whether persistently high levels of MMP activity in chronic lung diseases such as CF have a net destructive or beneficial effect.
Increased salivary syndecan-1 level is associated with salivary gland function and inflammation in patients with Sjögren’s syndrome
Published in Scandinavian Journal of Rheumatology, 2022
NY Lee, NR Kim, JW Kang, G Kim, M-S Han, JA Jang, D Ahn, JH Jeong, M-H Han, EJ Nam
Syndecan-1 (SDC-1) is a transmembrane heparin sulphate proteoglycan consisting of glycosaminoglycan chains including heparin sulphate and chondroitin sulphate, and core protein (4, 5). SDC-1 is predominantly expressed on epithelial and plasma cells (4, 5) and induced by growth factors (6, 7). SDC-1 functions primarily as a co-receptor by binding to and regulating numerous heparin sulphate-binding molecules, including growth factors, cytokines, chemokines, matrix molecules, and enzymes such as metzincin proteases, thereby affecting cell proliferation, adhesion, and motility (4, 5, 8). SDC-1 also exists in a soluble form through ectodomain shedding mediated by sheddases, such as matrix metalloproteinase (MMP)-2, MMP-3, MMP-7, MMP-9, and MMP-14 (4, 9, 10). SDC-1 ectodomain shedding constitutes an important regulatory mechanism because it rapidly changes surface receptor dynamics and generates soluble ectodomains that can behave as paracrine or autocrine effectors, or competitive inhibitors (4, 10). The shedding mechanism may be induced by inflammatory mediators, including cytokines, chemokines, growth factors, and cell stress (4, 5). Therefore, an inflammatory milieu with increased expression of such mediators along with MMPs (11–19) may induce SDC-1 shedding and alter SDC-1 expression on SGECs in the glands of patients with SS.