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Immunohistochemical Characterization of Extracellular Matrix in Tumor Tissues
Published in Róza Ádány, Tumor Matrix Biology, 2017
A large interstitial proteoglycan, versican, has been isolated from human fibroblast cultures.107 Versican has a large core protein (molecular weight approximately 260,000) with chondroitin sulfate or dermatan sulfate side chains. Proteoglycans resembling versican have been found in many other connective tissues. They are awaiting positive identification as versican or closely related members of a proteoglycan family (see review by Yanagishita, 1993).8 The antigen for 2B1 is considered to be a proteoglycan resembling versican.
Extracellular Matrix: The State of the Art in Regenerative Medicine
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Gurpreet Singh, Pooja A Chawla, Abdul Faruk, Viney Chawla, Anmoldeep Kaur
Pulmonary ECM is a structural complex system of protein molecules, which participate in various biochemical processes (Burgstaller et al. 2017). The remodelling mechanism is important for tissue homeostasis and any change in it may result in conditions like chronic obstructive pulmonary disease (COPD). Impaired expression of ECM proteins seen in COPD leads to the degradation and disruption of alveolar walls and stiffening of minor airways, which result in obstruction of airways (Ito et al. 2019). Alterations in ECM composition also influence the immune cell movement and their maintenance in the lung (Bonnans et al. 2014). Any abnormal functioning of ECM and response of inflammatory cell surface receptors may modify the collagen microstructure of the lung (Hussell et al. 2018). It is observed that there is a change in collagen organisation in COPD lung as compared to normal lung. The imbalance of enzymes like lysyloxidase and transglutaminase2 may involve structural changes of ECM during COPD (Burgess et al. 2016). ECM regulates normal interstitial fluid dynamics and strength and elasticity, tissue repair, and remodelling in the lungs. Versican and perlecan participate in the balancing of tissue fluid homeostasis (Pelosi et al. 2007). In the area of regenerative medicine, several studies reported lung scaffolds from small and large animals as an alternative to lung transplantation (Ohata and Ott 2020). These lung scaffolds were decellularised and reseed with lung perfusion culture in bioreactors. The resulting bioartificial lungs are probable to solve the problem of donor organ shortage and also reduced the immunogenicity (Panoskaltsis-Mortari 2015).
Decreased ADAMTS-1, -9 and -20 levels in women with endometrial polyps: a possible link between extracellular matrix proteases and endometrial pathologies*
Published in Journal of Obstetrics and Gynaecology, 2019
Aytekin Tokmak, Gulnur Ozaksit, Esma Sarikaya, Meryem Kuru-Pekcan, Arzu Kosem
ADAMTS-9 and -20 are known as Gon-ADAMTS (Somerville et al. 2003). The ADAMTS-9 gene located in the short arm of chromosome 3 is composed of 39 exons. Its protein consists of 1935 amino acids and weighs 216 kDa. Its main substrates are aggrecan and versican. Aggrecan and versican are large chondroitin sulphate proteoglycans which form major component of the ECM. Versican is primarily involved in cell adhesion, proliferation, migration and angiogenesis. It also has an essential role in tissue morphogenesis and maintenance. ADAMTS-9 protease is implicated in versican turnover during embryogenesis and even later periods of human life. Mouse genetic models have shown that versican is cleaved by ADAMTS9 (Dubail et al. 2014). Obesity, metabolic syndrome and diabetes are well-known risk factors for EP development (Özkan et al. 2015). ADAMTS-9 has also been associated with various anthropometric features, such as adiposity, obesity, type 2 diabetes, menarche age, as well as arrest of cervical dilatation during labour (Zeggini et al. 2008; Dubail and Apte 2015). In our study, no statistically significant differences were observed between the groups with regard to ADAMTS-1 and -20 levels. However, ADAMTS-9 was significantly lower in the study group compared to the controls. We can easily speculate that reduced ADAMTS-9 activity observed in women with EPs may cause EP formation by preventing ECM degradation or by increasing angiogenesis. However, ADAMTS-9 had a high sensitivity for predicting EPs whereas its specificity was low. Therefore, we think that is one of the most crucial metalloprotease waiting to be uncovered.
Versican modulates tumor-associated macrophage properties to stimulate mesothelioma growth
Published in OncoImmunology, 2019
Apostolos G. Pappas, Sophia Magkouta, Ioannis S. Pateras, Ioannis Skianis, Charalampos Moschos, Maria Eleni Vazakidou, Katherina Psarra, Vassilis G. Gorgoulis, Ioannis Kalomenidis
Mesothelioma tissue and pleural fluid, obtained from C57Bl/6 mice, were analyzed using flow cytometry, in order to explore the impact of versican on tumor-elicited immune response. Versican-deficient mesotheliomas contained fewer Tumor Associated Macrophages-TAMs (CD11b+ F4/80+) and Tumor Associated Neutrophils-TANs (CD11b+ GR1high), while the corresponding MPE contained fewer TAMs, TANs and CD8 + T-lymphocytes, compared to control tumor and MPE, respectively (Figure 4(a)). Furthermore, versican silencing shifted TAMs towards an anti-tumor M1 phenotype, as it is indicated by the significantly higher IL12:IL10 expression ratio, in versican-deficient tumors and corresponding MPEs, compared to control ones (Figure 4(b)). In addition, MPE CD4+ cells of mice bearing versican-expressing MPM tended to acquire a T regulatory cell (Treg) phenotype (CD4+ Foxp3+),16 while versican depletion in mesothelioma cells partially inhibited this effect (Figure 4(c)). Finally, versican silencing in cancer cells had no impact on CD8+ activation, determined by CD137 expression (data not shown). Overall, versican confers anti-tumor properties in tumor immune/inflammatory milieu.
The role of extracellular matrix components in angiogenesis and fibrosis: Possible implication for Systemic Sclerosis
Published in Modern Rheumatology, 2018
Vasiliki Liakouli, Paola Cipriani, Paola Di Benedetto, Piero Ruscitti, Francesco Carubbi, Onorina Berardicurti, Noemi Panzera, Roberto Giacomelli
Versican, a chondroitin sulfate PG, has a pivotal role in modulating cell behavior and ECM assembly. Versican, highly expressed in the early stages of development, is down-regulated after tissue maturation, although during wound repair or tumor angiogenesis, its expression is again up-regulated [54]. Smooth muscle cells (SMCs) have previously been demonstrated to be the main source of versican in blood vessels. Accordingly, versican was mainly found in the vascular ECM accumulated after vascular injury and promotes SMC proliferation in systemic arteries. Under hypoxic conditions, both versican messenger RNA expression and protein may be shown in the arterial neointima, and in plexiform lesions of patients with idiopathic PAH, as well as in PAH secondary to connective tissue disease. Thus, it has been supposed that versican promotes proliferation of pulmonary SMCs and vascular remodeling in PAH [54]. However, whether versican plays a functional role in PAH or alternatively, it is just part of the normal response of the vessels when there is a pathological insult still remains unknown. Furthermore, it has been shown that versican is a major component of the early fibroproliferative matrix in lung fibrosis where its deposition is associated with fibroblast migration and proliferation, preceding collagen deposition [55,56] and it is able to bind type I collagen and hyaluronic acid to maintain the integrity of the ECM. Furthermore, a higher synthesis of versican was observed in the fibroblasts of the sclerotic skin [57] and circulating monocytes from SSc patients thus, contributing to the fibrosis [58] (Table 1 and Figure 2).