lncRNA A05Rik是前期课题筛选获得，能通过调控靶基因HOXA3促百草枯致肺纤维化发展的一条新长链非编码RNA，但HOXA3非其唯一调控途径。通过Pulldown实验线索、AGO-RIP技术以及测序结果，我们筛选获得与A05Rik存在结合位点、低表达于百草枯动物和细胞模型的miRNA-1236。初步研究发现调控EMT关键基因IGFBP5是miRNA-1236下游靶基因；沉默A05Rik可致miR-1236表达升高、IGFBP5表达下降同时逆转EMT过程，且不受HOXA3影响。故提出A05Rik/miR-1236/IGFBP5通路促百草枯致肺纤维化的科学假说。本项目拟结合体内体外，交叉过表达/沉默策略，阐明lncRNA A05Rik吸附miR-1236调控IGFBP5表达的分子机制。有助于完整了解ncRNA-ncRNA网络参与百草枯致肺纤维化的机制，为治疗此疾病提供新靶标的证据。

lncRNA A05Rik was a novel long non-coding RNA identified from our previous subject. Which can up-regulated Paraquat induced pulmonary fibrosis process through mediated target gene HOXA3. However, HOXA3 wasn’t the exclusively pathway for A05Rik’s regulation. Combining the clue from Pull down results, the AGO-RIP as well as the RNA-Seq, we obtained a miRNA, miRNA-1236, which had several binding site with A05Rik, was significant lower expressed in Paraquat treated animal model and cells line samples. Preliminary data showed that miRNA-1236 target gene IGFBP5 was a key factor for the EMT regulation. Silence of A05Rik led to the higher expression of miR-1236, and lower expression of IGFBP5, thus reversed the EMT process, and that was happened without HOXA3. Those finding suggest that A05Rik/miR-1236/IGFBP5 pathway may accelerate Paraquat induced pulmonary fibrosis. The current study aims to illuminate the mechanism of adsorption effect between A05Rik and miR-1236, and the following IGFBP5 regulation both in vivo and in vitro using cross gain and loss-of-function approaches and might provide novel and integrated mechanism on ncRNA-ncRNA network in Paraquat induced pulmonary fibrosis and therapeutic strategies for treatment of the disease on its early stage.