Transforming growth factor-β1 induces intestinal myofibroblast differentiation and modulates their migration

Figure 9 Schematic illustration of the role of TGF-β1, FN, and FAK in the development of fibrosis in CD. After wounding TGF-β1 is produced by different cell types and connective tissue cells. CLPF increase FAK phosphorylation and migrate into the wound along the TGF-β1 gradient. FN that is also produced during migration induction and secreted at the site of injury may lead to an additional enhancement of the migratory gradient. Long term contact with TGF-β1 within the wound allows fibroblasts to differentiate into myofibroblasts. These cells have a reduced migratory potential and support wound healing via wound contraction and production of extracellular matrix deposition like FN. Phosphorylation of FAK is reduced after longer contact with TGF-β1 due to the differentiation into ECM-producing myofibroblasts.