长链非编码RNA转移相关肺腺癌转录本-1在高氧致新生鼠支气管肺发育不良中的表达及意义  

Expression and significance of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 in bronchopulmonary dysplasia of neonatal rats induced by hyperoxia

作　　者：范林 贾献献 吴波[1] 许巍[1] Fan Lin;Jia Xianxian;Wu Bo;Xu Wei(Department of Pediatrics,Shengjing Hospital of China Medical University,Shenyang 110004,China)

机构地区：[1]中国医科大学附属盛京医院儿内科,沈阳110004

出　　处：《中国小儿急救医学》2022年第5期368-372,共5页Chinese Pediatric Emergency Medicine

基　　金：辽宁省重点研发指导计划(2019JH8/10300023);国家自然科学基金(81771621);中国医科大学附属盛京医院"345人才工程"项目。

摘　　要：目的探讨长链非编码RNA转移相关肺腺癌转录本-1(lncRNA MALAT1)在高氧致新生大鼠支气管肺发育不良中的表达及其对肺泡Ⅱ型上皮细胞(AECⅡ)的作用。方法制备新生SD大鼠高氧致肺损伤模型(模型组,n=50,吸入氧浓度为80%~85%)及对照组(吸入空气,n=50)。在第1、3、7、14、21天取材并保留肺组织,应用石蜡包埋切片及苏木精-伊红染色检测肺组织的生理及病理改变;实时荧光定量聚合酶链式反应检测肺组织中lncRNA MALAT1的动态表达情况;Western blot检测肺组织及AECⅡ中表面活性蛋白C(SPC)的动态表达情况。从正常新生鼠肺组织提取AECⅡ,应用siRNA敲减lncRNA MALAT1,收集细胞并应用Western blot、免疫荧光检测SPC的变化。结果模型组肺组织逐渐出现肺泡间隔增厚,肺泡腔增大伴随肺泡棘消失等病理结构改变。与对照组比较,模型组大鼠肺组织中第1、3天lncRNA MALAT1、SPC表达无差异(P<0.05),第7、14、21天lncRNA MALAT1与SPC的表达明显升高,差异有统计学意义(P<0.05)。当lncRNA MALAT1受到抑制时,SPC表现出下调的趋势。结论高氧可导致新生大鼠肺发育的停滞,且肺泡结构紊乱及功能受损。LncRNA MALAT1的表达可能参与了高氧致新生鼠支气管肺发育不良的过程,lncRNA MALAT1的增加可能促进了AECⅡ的增殖。Objective To investigate the expression of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1)in bronchopulmonary dysplasia(BPD)of neonatal rats induced by hyperoxia and its effect on alveolar type 2 epithelial cells(AECⅡ).Methods The lung injury model of neonatal SD rats induced by hyperoxia(model group,n=50,inhaled oxygen concentration of 80%-85%)and the control group(inhaled air,n=50)were prepared.Lung tissue samples were taken and retained on days 1,3,7,14 and 21,and the physiological and pathological changes of lung tissue were detected by paraffin-embedded sections and hematoxylin-eosin staining;The dynamic expression of lncRNA MALAT1 in lung tissue was detected by real-time fluorescent quantitative polymerase chain reaction;The dynamic expression of surfactant protein C(SPC)in lung tissue and AECⅡwas detected by Western blot.AECⅡwas extracted from lung tissue of normal newborn rats,and lncRNA MALAT1 was knocked down by siRNA.The cells were collected and Western blot as well as immunofluorescence were used to detect the changes of SPC.Results The lung tissue of model group gradually became thickened with alveolar compartments,and the alveolar cavity was enlarged with the disappearance of alveolar spine and other pathological structural changes.Compared with the control group,there was no difference in the expression of lncRNA MALAT1 and SPC in the lung tissue from model group on days 1,3(P>0.05),but the expression of lncRNA MALAT1 and SPC significantly increased on days 7,14 and 21(P<0.05).When lncRNA MALAT1 was inhibited,SPC expression showed a decrease trend.Conclusion Hyperoxia can lead to the stagnation of lung development in neonatal rats,and the structure and function of alveolar disorders are impaired.The expression of lncRNA MALAT1 is involved in the process of hyperoxia-induced BPD in neonatal rats.The increase of lncRNA MALAT1 may promote the proliferation of AECⅡ.

关 键 词：支气管肺发育不良 肺泡Ⅱ型上皮细胞 长链非编码RNA转移相关肺腺癌转录本-1 增殖 大鼠 

分 类 号：R734.2[医药卫生—肿瘤]