In this study, we sought to learn whether the cross-talk between transforming growth factor-β (TGF-β), a central mediator in pulmonary fibrosis, and periostin in lung fibroblasts leads to generation of pulmonary fibrosis and whether inhibitors for integrin α<sub>V</sub>β<sub>3</sub>, a periostin receptor, can block pulmonary fibrosis in model mice and the TGF-β signals in fibroblasts from IPF patients.
The monomeric periostin levels can be used to predict pulmonary function decline and to distinguish IPF patients from healthy controls.In conclusion, periostin may play an important role in fibrogenesis and could be a potential biomarker for predicting disease progression and therapeutic effect in IPF patients.
Inhibition of periostin expression by giving an intratracheal antisense oligonucleotide targeting periostin mRNA was found to suppress bleomycin-induced lung fibrosis and thereby to attenuate metastatic colonization of the lung by melanoma cells.
Serum levels of periostin may predict clinical progression in this disease and periostin promotes myofibroblast differentiation and type 1 collagen production to contribute to aberrant lung fibrosis.
These findings suggest that direct administration of siRNA or antisense oligonucleotides against periostin into the lungs is a promising alternative therapeutic approach for the management of pulmonary fibrosis.