文章摘要
许家艳,孟亚奇,贾 嫚,姚 欣.人支气管上皮细胞表达的斯钙素⁃1在上皮间充质转化中的作用研究[J].南京医科大学学报,2018,(9):1198~1203
人支气管上皮细胞表达的斯钙素⁃1在上皮间充质转化中的作用研究
The effect of stanniocalcin⁃1 on epithelial⁃mesenchymal transition in bronchial epithelial cells
投稿时间:2018-03-29  
DOI:10.7655/NYDXBNS20180905
中文关键词: 斯钙素⁃1  人支气管上皮细胞  上皮间充质转化  慢性阻塞性肺疾病
英文关键词: STC1  human bronchial epithelial cells  EMT  COPD
基金项目:国家自然科学基金(81470237)
作者单位
许家艳 南京医科大学第一附属医院呼吸与危重症医学科江苏 南京 210029 
孟亚奇 南京医科大学第一附属医院呼吸与危重症医学科江苏 南京 210029 
贾 嫚 南京医科大学第一附属医院呼吸与危重症医学科江苏 南京 210029 
姚 欣 南京医科大学第一附属医院呼吸与危重症医学科江苏 南京 210029 
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中文摘要:
      目的:明确斯钙素?1(stanniocalcin?1,STC1)对支气管上皮间充质转化(epithelial?mesenchymal transition,EMT)的影响,以及香烟烟雾提取物(cigarette smoke extract,CSE)对支气管上皮细胞STC1表达调控的效应,探讨STC1在慢性阻塞性肺疾病气道EMT中的可能作用。方法:采用转化生长因子β(transforming growth factor β,TGF?β)处理人支气管上皮(16HBE)细胞72 h诱导EMT模型:外源加入STC1重组蛋白(rhSTC1),Western blot及免疫荧光法检测EMT标志物E?钙黏蛋白(E?cadherin)和α?平滑肌动蛋白(α?SMA)表达。采用CSE刺激16HBE细胞24 h:实时定量PCR及Western blot检测STC1 mRNA和蛋白表达差异,外源加入NF?κB抑制剂JSH23,Western blot检测STC1表达差异。结果:TGF?β可诱导16HBE细胞由典型的多边铺路石样变为长梭形,上皮细胞标志物E?cadherin表达下降,间质细胞标志物α?SMA表达增加,rhSTC1可逆转上述改变。CSE可刺激16HBE细胞STC1表达增高,且呈浓度依赖性增加,外源加入NF?κB抑制剂JSH23可抑制上述效应。结论:STC1在慢性阻塞性肺疾病形成过程中,是抑制气道EMT的保护性因素。CSE局部刺激支气管上皮细胞,通过NF?κB信号导致STC1反应性增加可能是其主要来源之一。
英文摘要:
      Objective:To investigate the effect of stanniocalcin(STC1) on epithelial?mesenchymal transition(EMT) in chronic obstructive pulmonary disease(COPD)and the expression in bronchial epithelial cells. Methods:Western blot and immunofluorescence were used to examine EMT associated biomarkers including E?cadherin and alpha smooth muscle actin(α?SMA). The STC1 mRNA and protein levels stimulated by cigarette smoke extract(CSE) in human bronchial epithelial(16HBE)cells were analyzed by real?time polymerase chain reaction(RT?PCR)and Western blot. Results:TGF?β induced EMT of 16HBE cells where the cell morphology changed from a typical multilateral paving stone?like appearance to a mesenchymal?like fusiform appearance along with the decreased expression of epithelium biomarker E?cadherin and the increased expression of mesenchymal cell markers α?SMA. rhSTC1 significantly inhibited the EMT changes mentioned above. The expression of STC1 was increased by CSE in a concentration?dependent manner in 16HBE cells. And this effect was inhibited by NF?κB inhibitor JSH23. Conclusion:STC1 was a protective factor to inhibit EMT during the development of COPD. CSE may stimulate bronchial epithelial cells,and increase the expression of STC1 through NF?κB signal,which may be the main source.
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