[No authors listed]
The tumor suppressor protein ELL-associated factor 2 (Eaf2) serves an important role in lens development and maturation; however, its role in oxidative stressâinduced cataract formation remains unclear. In the present study, an in vitro apoptosis model was constructed by treating HLEâB3 cells with 50 µM hydrogen peroxide (H2O2), and was confirmed by flow cytometry. Subsequently, overexpression of Eaf2 was induced in H2O2âinduced HLEâB3 cells by ligating Eaf2 cDNA to a pcDNA3.0 plasmid and the role of Wnt3a in the function of Eaf2 was also assessed by inhibiting the expression of the gene in Eaf2âoverexpression cells. The expression levels of glycogen synthase kinase 3β, βâcatenin, Eaf2, caspase 3, Wnt3a, Bâcell lymphoma 2 (Bclâ2) and Bclâ2âassociated X protein were examined using reverse transcriptionâquantitative polymerase chain reaction and western blot analysis. Immunocytochemistry was used to locate Eaf2 and Wnt3 protein expression in the H2O2âinduced HLEâB3 cells. The results indicated that Eaf2 was able to effectively suppress H2O2âinduced apoptosis of HLE cells via inhibition of caspase 3 production and activation of Wnt3a signaling. In addition, knockdown of Wnt3a in Eaf2âoverexpression cells evidently counteracted the effect of Eaf2 in antagonizing H2O2âinduced apoptosis. Taken together, these findings suggested that Eaf2 may suppress oxidative stressâinduced apoptosis of HLEâB3 cells exerted through the activation of Wnt3a signaling.
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