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Background To investigate the underlying mechanism of S100A4 function and whether it plays a role in retinal neovascularization(RNV)in a mouse model of oxygen-induced retinopathy(OIR).Methods Retinas from a mouse model of OIR were treated with and without an intravitreous injection of adenoviral-S100A4-RNAi or adenoviral-green fluorescence protein at postnatal day 12(P12).At P17,the efficacy of adenoviral gene transfer was assessed using fluorescence microscopy and western blot analysis.