肺泡上皮细胞凋亡在COPD的发生发展中起到重要的作用。LncRNAs从多个层面参与调节基因表达，影响分化、增殖及凋亡等细胞过程。前期研究发现COPD患者外周血中lncR-RP11-521C20.3表达降低，与其位置邻近的促凋亡基因BMF表达增高。通过生物信息学方法预测lncR-RP11-521C20.3的靶基因可能是与凋亡密切相关的BMF，进而对COPD患者及大鼠模型肺组织采用QPCR验证lncR-RP11-521C20.3和BMF的表达量，证实了前期结果，提示lncR-RP11-521C20.3可能在COPD的凋亡中起重要作用。本课题将通过构建肺泡上皮细胞凋亡模型研究低表达和过表达lncR-RP11-521C20.3/BMF对肺泡上皮细胞凋亡的影响，探讨lncR-RP11-521C20.3调控BMF信号通路在COPD肺泡上皮细胞凋亡中的作用机制，为COPD的防治提供新证据。

The apoptosis of alveolar epithelial cells plays a significant role in the occurrence and development of chronic obstructive pulmonary disease (COPD). LncRNAs participate in the regulation of gene expression, and influence the cellular processes of differentiation, proliferation, and apoptosis and so on from multiple levels. In previous studies, we found that the expression of lncR-RP11-521C20.3 in peripheral blood of COPD patients lowered while the expression of pro-apoptosis gene, BMF, adjacent to the location of lncR-RP11-521C20.3, increased. We predict that the target gene of lncR-RP11-521C20.3 might be the BMF which is closely related to the apoptosis by bioinformatics methods. And then we verified that the expressions of lncR-RP11-521C20.3 and BMF were the same as the result of previous studies by QPCR analysis, and that means lncR-RP11-521C20.3 might plays an important role in the apoptosis of COPD. In this study, the model of alveolar epithelial cells apoptosis will be constructed, and then we will study the effect of overexpression and low-expression of lncR-RP11-521C20.3/ BMF on alveolar epithelial cells apoptosis, investigate the mechanisms of lncR-RP11-521C20.3 on alveolar epithelial cells apoptosis by regulating BMF signal pathway, and thus provide new evidence for the prevention and treatment of COPD.