RGD-Dependent Epithelial Cell-Matrix Interactions in the Human Intestinal Crypt

Figure 5

Regulation of dynamic assembly of fibronectin by type VI collagen. Schematic representation of the proposed mechanism by which collagen VI regulates FN fibrillogenesis. In HIEC, collagen VI is deposited into the ECM and interferes with fibronectin assembly by three distinct mechanisms. (a) First, in HIEC collagen VI competes with fibronectin for β1 integrin binding in focal adhesions. (b) Second, collagen VI limits cellular accessibility of fibronectin through a direct interaction with FN preventing fibronectin association with other fibronectin molecules, a step required for the extensive formation of the fibronectin matrix. (c) The third mechanism involves the regulation of MLCK by collagen VI. When collagen VI is depleted from the ECM, the MLCK/MLC pathway is activated by an unknown mechanism and mediates fibrillar actin contractility that allows the recruitment of tensin to FBs generating extensive fibrillogenesis. The increase in fibronectin deposition followed the depletion of collagen VI is accompanied by an increase in migration.