Collagens I and V differently regulate the proliferation and adhesion of rat islet INS-1 cells through the integrin beta 1/E-cadherin/beta-catenin pathway.

Extracellular matrix (ECM) plays an important role in tissue repair, cell proliferation, and differentiation. Our previous study showed that collagen I and collagen V differently regulate the proliferation of rat pancreatic beta cells (INS-1 cells) through opposite influences on the nuclear translocation of beta-catenin. In this study, we investigated the beta-catenin pathway in INS-1 cells on dishes coated with collagen I or V. We found that nuclear translocation of the transcription factor Yes-associated protein (YAP) was enhanced by collagen I and suppressed by collagen V, but had no effect on INS-1 cell proliferation. Morphologically, INS-1 cells on collagen V-coated dishes showed stronger cell-to-cell adhesion, while the cells on collagen I-coated dishes showed weaker cell-to-cell adhesion in comparison with the cells on non-coated dishes. E-cadherin played an inhibitory role in the proliferation of INS-1 cells cultured on collagen I or collagen V coated dishes via regulation of the nuclear translocation of beta-catenin. Integrin beta 1 was enhanced with collagen I, while it was repressed with collagen V. The integrin beta 1 pathway positively regulated the cell proliferation. Inhibition of integrin beta 1 pathway restored the protein level of E-cadherin and inhibited the nuclear translocation of beta-catenin in the cells on collagen I-coated dishes, but no effect was observed in the cells on collagen V-coated dishes. In conclusion, collagen I enhances the proliferation of INS-1 cells via the integrin beta 1 and E-cadherin/beta-catenin signaling pathway. In INS-1 cells on collagen V-coated dishes, both integrin beta 1 and E-cadherin/beta-catenin signal pathways are involved in the inhibition of proliferation.