晶状体上皮间质转化（EMT）是后发性白内障（PCO）的主要病理改变。课题组前期研究显示：miR-204和miR-30a 是人、小鼠和大鼠PCO组织共同差异表达的miRNA；其预测的靶基因包括Smad4、Smad5、MAPK1、Snail1/2和ZEB1等，涉及了EMT发生的三条主要信号途径，且前期工作证实miR-204及其靶基因Smad4通过Smad途径显著调控PCO中EMT进程。本研究将完善大鼠PCO不同时间miRNA差异表达谱，以miR-30a与miR-204为主要研究对象，结合生物信息学，应用报告基因系统、Western blot、定量PCR、免疫荧光以及干扰RNA等技术，利用囊袋培养和PCO动物模型研究上述miRNAs调控晶状体上皮细胞EMT的作用机制以及通过miRNAs干预PCO的可行性。本项目从转录后水平探讨PCO发病机制，以期为防治PCO提供新的研究思路和干预手段。

A secondary cataract, also termed as posterior capsular opacification (PCO), is the most common complication of cataract surgery. Following the insult of surgery, residual lens epithelial cells (LECs) rapidly grow at the equator and under the anterior lens capsule. This condition is known as PCO. The remaining LECs undergo an epithelial-to-mesenchymal transition (EMT), resulting in the formation of fibroblasts instead of normal differentiation into lens fiber cells. EMT is the principal pathological change of PCO after lens extracapsular extraction. According to previous studies, miR-30a and miR-204 are the common part of microRNAs differential expression profile of PCO in human, mouse and rat. The predicted target genes conclude Smad4、Smad5、MAPK1、Snail1/2 and ZEB1, which belong to the major signal pathways involved in SMADs pathway, MAPK/ERK Kinase signaling pathway, and transcription factors pathway. All of these pathways are the main and key pathways of EMT. In the previous studies, we also found that miR-204 directly regulates EMT through its targeting of SMAD4. Therefore, in this study we will use capsular bag cultivation model in vitro and PCO animal model in vivo to further investigate the regulational mechanisms of miRNAs in EMT of PCO. We are going to comlpete the differential expression profiling of microRNAs on rat PCO, and to investigate the role of miR-30a and miR-204 in regulating EMT during PCO by using bioinformatics, luciferase reporter gene systerm, Western blot, real-time PCR, immunofluorescence, and siRNA techniques. We hope this study will help to move forward a further step to give a novel insight of molecular mechanisms of PCO and find some novel targets for PCO therapeutic intervention.