Abstract

PURPOSE: Idiopathic pulmonary fibrosis (IPF) is the most common and most aggressive form of idiopathic interstitial pneumonia. Transforming growth factor beta (TGF-β) has been shown to be a particularly important mediator of fibroblast proliferation and extracellular matrix (ECM) production in IPF lungs. Interferon gamma-1b (IFN-γ 1b) inhibits TGF-β-induced collagen synthesis by up-regulating SMAD7 expression and inducing formation of an inhibitory RFX5 complex on the collagen promoter region. We recently discovered that pirfenidone exerts antifibrotic effects by inhibiting p38 MAPK, an essential intracellular mediator of TGF-β-induced collagen synthesis. Given their distinctive modes of action against TGF-β-induced collagen expression, we wanted to determine whether the concomitant administration of IFN-γ 1b and pirfenidone would result in complementary or antagonistic effects against TGF-β-induced gene induction in human lung fibroblasts (HFL-1).

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.