Inflammation Location, But Not Type, Determines the Increase in TGF-β1 and IGF-1 Expression and Collagen Deposition in IBD Intestine
Autor: | Lesley Maxwell, William F. Doe, Ian Craig Lawrance |
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Rok vydání: | 2001 |
Předmět: |
Pathology
medicine.medical_specialty Inflammation In situ hybridization Inflammatory bowel disease Transforming Growth Factor beta1 Extracellular matrix Collagen Type III Transforming Growth Factor beta Fibrosis medicine Humans Immunology and Allergy Insulin-Like Growth Factor I Lamina propria Chemistry Gastroenterology Inflammatory Bowel Diseases medicine.disease Immunohistochemistry medicine.anatomical_structure Gene Expression Regulation Collagen medicine.symptom Transforming growth factor |
Zdroj: | Inflammatory Bowel Disease. 7:16-26 |
ISSN: | 1078-0998 |
DOI: | 10.1097/00054725-200102000-00003 |
Popis: | Background and Aims Inflammatory bowel disease (IBD) is frequently complicated by extracellular matrix (ECM) changes that may result in fibrosis. Transforming growth factor (TGF)-β1 and insulin-like growth factor (IGF)-1 mediate numerous ECM changes. Our aim was to determine whether TGF-β1 and IGF-1 are involved in intestinal ECM collagen regulation and what impact the inflammatory infiltrate has on their expression. Methods TGF-β1 and IGF-1 mRNA and protein were assessed in fibrosed Crohn's disease (CD), inflamed CD, inflamed ulcerative colitis (UC), and control intestine using in situ hybridization and immunohistochemistry. Collagen types I and III were quantified by electron immunohistochemistry. Results In CD, increased TGF-β1 and IGF-1 mRNA expression was transmural. In UC, the increase was confined to the lamina propria and submucosa. In both, distribution of TGF-β1 and IGF-1 protein matched mRNA expression and coincided with the distribution of the inflammatory infiltrate. An increase in the collagen type III:I ratio in both CD and UC also coincided with the inflammatory infiltrate. Conclusions These findings suggest that TGF-β1 and IGF-1 are involved in intestinal ECM remodeling in IBD, and their enhanced expression depends on the presence and location of inflammatory infiltrates rather than the type of IBD. |
Databáze: | OpenAIRE |
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