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Pirfenidone reduces fibronectin synthesis by cultured human retinal pigment epithelial cells
S Zhang1, I A Shiels, J S Ambler
1Department of Physiology and Pharmacology, University of Queensland, Brisbane, Australia. zhang@plpk.uq.oz.au
Purpose:
Pirfenidone is a novel anti-fibrotic drug that has been shown to inhibit fibroblast growth and collagen synthesis induced by transforming growth factor (TGF)-beta1. In the present study we investigated the ability of pirfenidone to moderate fibronectin synthesis by cultured human retinal pigment epithelial (RPE) cells maintained in media containing 1% foetal bovine serum when stimulated with TGF-beta1.
Methods:
Primary human RPE cultures were used. Treatments included TGF-beta1, pirfenidone and pirfenidone with TGF-beta1. After 72 h treatments, cell growth was determined by cell counting and fibronectin was measured by ELISA.
Results:
Transforming growth factor-beta1 (1-10 ng/mL) increased the production of soluble fibronectin, while pirfenidone (300 micromol/L) significantly reduced the TGF-beta1-induced synthesis of fibronectin. Pirfenidone alone had no effect on fibronectin synthesis by cultured RPE cells.
Conclusion:
We conclude that the anti-fibrotic effect of pirfenidone may be partly mediated through inhibition of TGF-beta1-induced fibronectin synthesis.