Brimonidine reduces TGF-beta-induced extracellular matrix synthesis in human Tenon’s fibroblasts

BACKGROUND: Brimonidine is a highly selective α(2) adrenergic agonist that has been widely used in anti-glaucoma eyedrops. The aim of this study was to investigate its putative anti-fibrotic role in the fibrosis caused by activated Tenon’s fibroblasts. METHODS: Primary cultured human Tenon’s fibroblasts were exposed to 2.0 ng/mL of transforming growth factor-β1 (TGF-β1) for up to 48 h. In the presence of various concentrations of brimonidine (from 0.0 to 10.0 μM), the expression levels of fibronectin, collagen types I and III, and β-actin were determined by Western immunoblots. The expression of phosphorylated SMAD2/3 (p-SMAD2/3) was then evaluated using immunofluorescence. RESULTS: TGF-β1 significantly increased the synthesis of fibronectin and collagens in human Tenon’s fibroblasts; however brimonidine treatment distinctly attenuated the TGF-β1-induced production of extracellular matrix (ECM) proteins. TGF-β1 also changed the cellular morphology to be plump, while brimonidine treatment returned the cells to a spindle shape, similar to control fibroblasts. Regarding p-SMAD2/3, brimonidine treatment did not show any apparent changes in its expression. CONCLUSIONS: Our data revealed that brimonidine reduces TGF-β-induced ECM synthesis in human Tenon’s fibroblasts in vitro. This finding implies that topical administration of brimonidine may be helpful in reducing the fibrosis caused by the long-term use of topical anti-glaucoma medications. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12886-015-0045-8) contains supplementary material, which is available to authorized users.