Foshan Chancheng Central Hospital, Foshan, Guangdong, China.
Cell Transplant. 2020 Jan-Dec;29:963689720918294. doi: 10.1177/0963689720918294.
Bronchopulmonary dysplasia (BPD), also known as neonatal chronic lung disease, is an important cause of respiratory illness in preterm newborns that results in significant morbidity and mortality. Long noncoding RNAs (lncRNAs) have been discovered with many biological functions. However, the role of lncRNAs in the pathogenesis of BPD remains poorly understood. Here, we established a mouse lung injury model that mimicked human BPD. Subsequently, we found the lncRNA H19 expression level was significantly increased in BPD compared with normal lung tissues using quantitative real-time polymerase chain reaction. Next, we observed that overexpression of lncRNA H19 enhanced mitogen-activated protein kinase (MAPK) signaling pathway. In addition, we also found that dysfunction of lncRNA H19 altered the expression of inflammatory factors. Thus, our study validates that lncRNA H19 contributes to the progression of BPD by regulating MAPK signaling pathway, which could be used as a potential target for treating BPD.
支气管肺发育不良(BPD),又称新生儿慢性肺疾病,是导致早产儿呼吸疾病的重要原因,其发病率和死亡率都很高。长链非编码 RNA(lncRNA)具有多种生物学功能已被发现。然而,lncRNA 在 BPD 发病机制中的作用仍知之甚少。在这里,我们建立了一个模拟人类 BPD 的小鼠肺损伤模型。随后,我们通过实时定量聚合酶链反应发现,与正常肺组织相比,BPD 中 lncRNA H19 的表达水平显著升高。接下来,我们观察到 lncRNA H19 的过表达增强了丝裂原活化蛋白激酶(MAPK)信号通路。此外,我们还发现 lncRNA H19 的功能障碍改变了炎症因子的表达。因此,我们的研究证实,lncRNA H19 通过调节 MAPK 信号通路促进 BPD 的进展,可作为治疗 BPD 的潜在靶点。