白内障是我国人口老龄化最严峻的问题之一。以手术为主的治疗模式已经远远不能满足数量剧增的白内障患者的复明需求，而发病机制不明确却严重限制着非手术治疗的发展。近年来，表观遗传学的发展为我们提供了新的思路。MircoRNAs（miRNAs）是长度为21-25nt 的小分子 RNA，通过碱基互补原则与目标 mRNA 结合并抑制其翻译，进而下调相应基因的表达引起相应病理生理改变；在前期实验中我们已经检测到miRNA-145在正常和年龄相关性白内障的晶状体中表达差异显著，并预测到其可调节晶状体发育相关基因E2F3的表达。然而，miRNA-145影响E2F3功能的分子机制尚未明确，与年龄相关性白内障发生病理改变的关系也需进一步的实验。因此，我们拟通过分子生物学技术探索miRNA-145对E2F3功能影响的具体机制，同时验证miR-145是否可以通过调节晶状体细胞的E2F3的表达，而导致白内障的发生。

Cataract is one of the severest problems of an aging population in China. Operation as the predominant treatment modality is far from meeting the demand of sharp increase in the amount of cataract patients. The development of non-operation treatment is restricted by etiological uncertainty. For the past few years, Epigenetics provide new insights into the etiology of cataract. MircoRNAs(miRNAs) is one kind of small RNAs with 21-25nt length, it can pair with mRNA to suppress translation, and result in pathological changes by repressing genes expression. In our previous experiments, it has been observed that miR-145 had obviously different expression between transparent and cataractous human lens. By using prediction algorithms, E2F3 which is involved in development of lens was been predicted to be regulated by miR-145. However, molecular mechanisms of E2F3' function affected by miR-145 are not clear, further research needed to identify the relationships between miR-145 and formation of cataract. Based on the above reasons, we will explore the mechanisms of miR-145 on E2F3 by molecular biotechnology, and also validate whether miR-145 would cause cataract by regulating E2F3 in lens epithelium cells.