Ratzinger, Sabine and Eble, Johannes A. and Pasoldt, Anja and Opolka, Alfred and Rogler, Gerhard and Grifka, Joachim and Graessel, Susanne (2010) Collagen XVI induces formation of focal contacts on intestinal myofibroblasts isolated from the normal and inflamed intestinal tract. MATRIX BIOLOGY, 29 (3). pp. 177-193. ISSN 0945-053X, 1569-1802
Full text not available from this repository. (Request a copy)Abstract
In Crohn's disease (CD) the stress-shield of intestinal subepithelial myofibroblasts (ISEMF) provided by intact tissue is disturbed due to inflammation and thus, cells start with remodelling activities. This is characterized by increased numbers of collagen-producing ISEMF causing an uncontrolled, irreversible wound-healing response to the chronic inflammation of the gastrointestinal tract. Reconstitution of the original ECM leads ISEMF to exit this cycle. In contrast, during fibrosis, ISEMF persist. It is known that ISEMF produce and deposit collagen types I, III, IV and V; however synthesis and the role of fibrillar peripheral molecules like collagen type XVI have not been addressed yet. Here, we have analyzed the distribution of collagen XVI in the normal and inflamed bowel wall, its gene and protein expression by ISEMF of different inflammation stages, the cell-matrix interactions in different phases of the inflammatory process and their effect on cell spreading, proliferation and migration. Collagen XVI is deposited in the submucosa of the intestinal wall where it co-localizes with fibrillin-1 and integrin alpha 1. ISEMF reveal increasing gene and protein expression of collagen XVI concurrent to increasing inflammation. ISEMF reveal more mature focal adhesion contacts when seeded on collagen XVI resulting in an extensive cell spreading. This involves recruitment of alpha 1 beta 1 integrin, which shows increased cell surface expression on ISEMF in late stages of inflammation. We assume that collagen XVI promotes persistence of ISEMF in the normal and, even stronger in the inflamed bowel wall by stabilizing focal adhesion contacts via cell-matrix interaction preferentially through recruitment of alpha 1 beta 1 integrin into the tips of the focal adhesion contacts. (C) 2009 Elsevier B.V. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CROHNS-DISEASE; EXTRACELLULAR-MATRIX; GRANULATION-TISSUE; CELL-PROLIFERATION; REDUCED EXPRESSION; FIBROBLASTS; INTEGRIN; FIBRONECTIN; ADHESION; ALPHA-2-BETA-1; Crohn's disease; Collagen XVI; Myofibroblast; Integrin; Fibrillin-1; Focal adhesion contact; Inflammation |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Orthopädie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 03 Aug 2020 09:07 |
| Last Modified: | 03 Aug 2020 09:07 |
| URI: | https://pred.uni-regensburg.de/id/eprint/24928 |
Actions (login required)
 |
View Item |
