Abstract
Fibrosis is an important feature of inflammatory bowel diseases (IBD), but its pathogenesis is incompletely understood. Our aim was to identify genes important for fibrosis in IBD by comparison with kidney and liver fibrosis. First, we performed bioinformatics analysis of Gene Expression Omnibus datasets of liver and kidney fibrosis and identified CXCL9, THBS2, MGP, PTPRC, CD52, GZMA, DPT and DCN as potentially important genes with altered expression in fibrosis. We then performed qPCR analysis of the selected genes’ expression on samples of fibrotic kidney, liver, Crohn’s disease (CD) with and without fibrosis and ulcerative colitis (UC), in comparison to corresponding normal tissue. We found significantly altered expression in fibrosis for all selected genes. A significant difference for some genes was observed in CD with fibrosis in comparison to CD without fibrosis and UC. We conclude that similar changes in the expression of selected genes in liver, kidney fibrosis and IBD provide further evidence that fibrosis in IBD might share common mechanisms with other organs, supporting the hypothesis that fibrosis is the common pathway in diseases of various organs. Some genes were already active in IBD with inflammation without fibrosis, suggesting the early activation of profibrotic pathways or overlapping function in fibrosis and inflammation.
Highlights
Intestinal fibrosis is a common feature in inflammatory bowel diseases (IBD), in Crohn’s disease (CD) [1,2]
DPT, were part of or connected to extracellular matrix and its organization, while on the other side we selected PTPRC, CD52, GZMA and CXCL9, which are involved in the immune response through different regulation mechanisms of T cells
Four genes with a direct interaction with COL1A1, MGP, THBS2, DCN and DPT, were part of or connected to extracellular matrix and its organization, while on the other side we selected PTPRC, CD52, GZMA and CXCL9, which are involved in the immune response through different regulation mechanisms of T cells
Summary
Intestinal fibrosis is a common feature in inflammatory bowel diseases (IBD), in Crohn’s disease (CD) [1,2]. Despite significant progress in the treatment of CD with anti-inflammatory agents, there is little impact on the incidence of fibrosis and intestinal strictures that necessitate surgical intervention [2,4,5,6]. Fibrosis is not unique to the bowel; it occurs in many organs, including the liver, kidney, heart, skin and lung. It is the end result of tissue damage and chronic injury, regardless of the involved organ [11]. There are many common mediators and signaling pathways involved in fibrosis, the most important being the transforming growth factor β (TGF-β) pathway, platelet-derived growth factor receptors (PDGFR) pathway, connective tissue growth factor (CTGF) pathway and others [11]
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