Abstract
ELL-associated factor 2 (Eaf2) has an important role in crystalline lens development and maturation; however, its role in ultraviolet radiation (UV)-induced cataract formation has remained elusive. The present study compared UV-induced cell apoptosis, activation of caspase-3 and caspase-9 and changes in protein expression levels of B-cell lymphoma 2 (bcl-2), bcl-2-associated X protein (bax) and phosphorylated extracellular signal-regulated kinase in wild-type and Eaf2-knockout mice. The results showed that Eaf2 knockout can reduce UV-induced apoptosis in crystalline lenses and mitigate the formation of cataracts. Further functional studies indicated that Eaf2 can induce the activation of caspase-3 and caspase-9, increase the protein expression of the pro-apoptotic protein bax and inhibit the expression of the anti-apoptotic protein bcl-2; thereby, Eaf2 promotes cell apoptosis and is implicated in the formation and development of cataracts. The present study laid a theoretical foundation for the development of drugs for cataract treatment.