Pioglitazone inhibits TGFβ induced keratocyte transformation to myofibroblast and extracellular matrix production

摘要: Phenotype transformation of corneal keratocyte to myofibroblast plays an important role in the wound healing process cornea and TGFβ is considered be most mediator induce trans-differentiation. Peroxisome proliferator-activated receptors-γ (PPAR-γ) activation has been proved exert anti-fibrotic effect many tissues. In this study, we investigated PPAR-γ agonist, pioglitazone, on transformation, extracellular matrix production cell proliferation. The results showed pioglitazone inhibited TGFβ-driven differentiation, as determined by F-actin fluorescence staining, α-smooth muscle actin-specific immunocytochemistry western blot analysis. Pioglitazone also potently attenuated induced type I collagen fibronectin mRNA protein production. Moreover, inhibitory irreversible antagonist GW9662, partially reversed inhibition expression but not suggesting both dependent independent mechanisms were involved action pioglitazone. Therefore, our study indicates a potential application therapy fibrosis might promising target.