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• W2170559268 abstract "Introduction The extracellular matrix is a complex, three-dimensional network of secreted molecules that provides structural support to tissues and environmental cues to the cells within. One particular subset of matrix molecules is specifically expressed upon tissue damage. These molecules contribute to effective tissue repair by orchestrating the behaviour of cells that mediate this process, and once the repair is complete, the expression of this matrix is down-regulated. Here, we focus on the recent data that highlights a direct role for injury-induced matrix molecules in driving inflammation upon tissue damage and propose that this matrix creates a specific microenvironment or ‘pro-inflammatory niche’ that is permissive for localized inflammation during repair. We also examine the evidence indicating that this niche exists, and persists, in the damaged joint of rheumatoid arthritis patients. Finally, we assess the data which demonstrate that these matrix molecules actively contribute to maintaining chronic inflammation during disease progression. Conclusion Together these findings imply that targeting the pro-inflammatory niche in the joint may provide a novel treatment strategy for rheumatoid arthritis. Introduction The extracellular matrix (ECM) is a complex organization of secreted molecules. The major constitutive components of the ECM include collagens, elastin, fibronectin, hyaluronic acid and proteoglycans. Together these molecules form a network that provides structural support for tissues and delivers environmental signals that regulate cell behaviour. However, there exists a unique subset of ECM molecules that are not constitutively expressed. Found at high levels during development, but absent from most healthy adult tissues, these proteins are specifically induced at sites of tissue injury. These molecules have been termed ‘matricellular proteins’ and include the CCN family (CCN1-6), galectins (Gal), fibulins, osteopontin (OPN), periostin, secreted protein acidic and rich in cysteine (SPARC), small leucine rich proteoglycans (SLPRs), tenascin-C (TNC) and thrombospondins-1 and -2 (TSP-1/2). Despite their structural diversity, these molecules possess a number of defining common features in addition to their distinct pattern of expression. They are key orchestrators of cell behaviour; this is mediated by their multimodular structure, which confers the ability to interact with a large number of diverse binding partners such as cell surface receptors, other ECM molecules, hormones, growth factors and cytokines. Moreover, they exert control over a wide range of cell functions in a highly contextand cell type-specific manner. Finally, although highly expressed during development, mice with targeted disruptions in these genes exhibit grossly normal phenotypes until subjected to tissue injury, whereupon they exhibit abnormal tissue repair. There is a large body of evidence supporting a major role for these proteins in driving the response to tissue injury1,2. The aim of this review is to discuss how the ECM drives persistent inflammation upon tissue damage to the joint in rheumatoid arthritis (RA). Discussion The authors have referenced some of their own studies in this review. These referenced studies have been conducted in accordance with the Declaration of Helsinki (1964), and the protocols of these studies have been approved by the relevant ethics committees related to the institution in which they were performed. All human subjects, in these referenced studies, gave informed consent to participate in these" @default.
• W2170559268 created "2016-06-24" @default.
• W2170559268 creator A5006506602 @default.
• W2170559268 creator A5061361019 @default.
• W2170559268 date "2013-03-01" @default.
• W2170559268 modified "2023-09-24" @default.
• W2170559268 title "The pro-inflammatory niche: how the extracellular matrix drives rheumatoid arthritis?" @default.
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