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Osamu Yamanaka, Winston W Y Kao, Shizuya Saika; Effects of β-catenin inhibitor, ICG-001, on cultured human conjunctival fibroblast. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3200.
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© ARVO (1962-2015); The Authors (2016-present)
To examine if a β-catenin inhibitor, ICG-001, modulates wound healing-related behaviors of cultured human subconjunctival fibroblasts. Transforming growth factor-β (TGF-β) signal, the major signal involved in conjunctival scarring, is know to be further regulated by β-catenin /Wnt signal.
(1) Immunohistochemical expression pattern of β-catenin in healing conjunctival tissue was examined in B57/BL6 mice. (2) Effects of adding ICG-001 on cell migration, expression of extracellular matrix (ECM), i. e., type I collagen and fibronectin, and expression of α-smooth muscle actin (α-SMA), were examined in cell culture with or without TGFβ1. Immunohistochmeistry, ELISA, or real-time RT-PCR was employed. Cell migration was examined using an in vitro scratch assay model in monolayer cultures.
(1) At day 2 and 5 post-injury, β-catenin immunoreactivity was strongly detected both in cytoplasm and nuclei of the fibroblasts then diminished in the injured conjunctiva. (2) ICG-001 markedly reduced expression of type I collagen, fibronectin and α-SMA in the cells treated with exogenous TGFβ1 but did not show any effects on the cells in the absence of TGFβ1. ICG-001 did not inhibit cell migration in the absence of TGFβ1, but counteracted the acceleration of cell migration by exogenous TGFβ1.
β-catenin signal is activated in fibroblasts at the injury in mouse conjunctiva. ICG-001, β-catenin inhibitor negatively modulates TGFβ1 acceleration of cell migration and expression of structural extracellular matrix. Inhibition of β-catenin signal could be a novel therapeutic strategy in preventing undesirable bleb scar formation during healing following filtration surgery.
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