Jiang Yanhua, Fu Rongrong, Zhao Jiangyue, Wu Di, Qiao Guang, Li Ruoxi, Zhang Jinsong
Department of Ophthalmology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning 110005, P.R. China.
Department of Ophthalmology, The Fourth People's Hospital of Shenyang, Shenyang, Liaoning 110031, P.R. China.
Mol Med Rep. 2015 Nov;12(5):6605-11. doi: 10.3892/mmr.2015.4281. Epub 2015 Sep 2.
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.
ELL相关因子2(Eaf2)在晶状体发育和成熟过程中发挥着重要作用;然而,其在紫外线(UV)诱导的白内障形成中的作用仍不明确。本研究比较了野生型和Eaf2基因敲除小鼠中紫外线诱导的细胞凋亡、半胱天冬酶-3和半胱天冬酶-9的激活以及B细胞淋巴瘤2(bcl-2)、bcl-2相关X蛋白(bax)和磷酸化细胞外信号调节激酶蛋白表达水平的变化。结果表明,Eaf2基因敲除可减少紫外线诱导的晶状体细胞凋亡并减轻白内障的形成。进一步的功能研究表明,Eaf2可诱导半胱天冬酶-3和半胱天冬酶-9的激活,增加促凋亡蛋白bax的蛋白表达并抑制抗凋亡蛋白bcl-2的表达;因此,Eaf2促进细胞凋亡并与白内障的形成和发展有关。本研究为白内障治疗药物的开发奠定了理论基础。