Additionally, we observed a concomitant increase in TIMP-1, the main inhibitor of MMP-1 (as well as MMP-2 and −9), and in type I collagen gene expression, suggesting that osteopontin may facilitate a profibrotic environment not only by its effect on epithelial cells but also by inducing a nondegradative microenvironment similar to the one observed in IPF and experimental lung fibrosis [36,37]. Here, MMP1 is linked to pulmonary fibrosis.