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S.-W. Chang, T.-C. Chen, T.-Y. Wang, S.-F. Chou; Moxifloxacin Suppresses Myofibroblast Differentiation via Blocking TGF-betaRI on Corneal Fibroblasts. Invest. Ophthalmol. Vis. Sci. 2010;51(13):362.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether moxifloxacin (MOX) modulates alpha smooth muscle actin (α-SMA) expression, a significant marker of myofibroblast differentiation, in corneal fibroblasts.
Primary human corneal fibroblasts were incubated in DMEM containing 0.1 mg/ml of MOX and/or 2 ng/ml transforming growth factor (TGF)-β1. The cells were harvested at 72 hours after incubation and the cell proliferation capability was analyzed through determination of cellular DNA using PicoGreen assay. The cytotoxicity was analyzed by LDH assay. The transcript and protein expression of α-SMA were determined by quantitative real-time PCR and Western blot, respectively. The α-SMA filaments were observed by fluorescent confocal microscopy. The number of TGF-betaRI on the fibroblast surface was analyzed by flow cytometry.
MOX 0.1 mg/ml had no significant effect on the proliferation and cytotoxicity of corneal fibroblasts both in the presence and absence of TGF-β1. In addition, MOX obviously prohibit the TGF-β1-induced α-SMA expression at both transcripts and protein levels. The α-SMA filaments could not be found in MOX-incubated corneal fibroblasts, even in the TGF-β1 containing culture medium. Moreover, MOX significantly blocked the expressions of TGF-betaRI induced by TGF-β1.
MOX inhibited polymerization of α-SMA filaments through blocking TGF-betaRI expressions on corneal fibroblasts.
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