Reduced migration of fibroblasts in inflammatory bowel disease: role of inflammatory mediators and focal adhesion kinase.
作者： Sandra Nicole Leeb , Daniela Vogl , Manuela Gunckel , Stephan Kiessling , Werner Falk
DOI: 10.1016/J.GASTRO.2003.07.004
关键词: Autophosphorylation 、 Tumor necrosis factor alpha 、 Pathology 、 Focal adhesion 、 Biology 、 Blot 、 Kinase 、 Molecular biology 、 Fibroblast 、 Inflammatory bowel disease 、 Lamina propria
摘要: Abstract Background & Aims: Crohn's disease (CD) and ulcerative colitis (UC) are associated with chronic tissue damage continuous repair. A central, but not well-characterized, event during this process is the migration of activated fibroblasts to wound. Methods: Human colonic lamina propria (CLPF) were isolated from patients CD UC healthy controls characterized by immunocytochemistry. Migration assays CLPF performed in modified 48-well Boyden chamber. Focal adhesion kinase (FAK) FAK autophosphorylation migrating determined Western blotting. mRNA expression was investigated Northern Results: The CD-CLPF UC-CLPF significantly reduced when compared control-CLPF. This correlated a decrease phosphorylation, whereas, control-CLPF, an increase found. Similarly, presence inflammatory mediators interferon (IFN)-γ (50 ng/mL) or tumor necrosis factor (TNF) (30 conditioned medium control-CLPF 41% ± 4% 30% 7%, respectively. Preincubation TNF (20 IFN-γ (10 for 3 days their migratory response 10% control ( P Conclusions: CD- have potential normal CLPF. That may be caused contact TNF. loss diminished phosphorylation.
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