检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:黄振杰[1] 郑金旭[2] 莫凯天[1] 苏石芳[1] 许世锋[1] 汤艳[2] 石益海[3]
机构地区:[1]广西北海市人民医院呼吸科,广西北海536000 [2]江苏大学附属医院呼吸科,江苏镇江212001 [3]上海市第八人民医院消化科,上海200235
出 处:《吉林医学》2010年第29期5062-5064,共3页Jilin Medical Journal
基 金:卫生部科研基金(编号:wkj2006-2-026);江苏省"333工程"基金(苏人才办2007-16-09)
摘 要:目的:通过观察TGF-β1诱导下A549细胞出现的细胞形态学和E-cad表达的变化,探讨上皮细胞-间质细胞转化(epithelial-mesenchymal transition,EMT)过程在肺纤维化发病机制中的作用。方法:体外培养A549细胞,以TGF-β1进行干预,收集不同时段的细胞,应用荧光实时定量PCR(RT-PCR)检测TGF-β1干预前后E-cad的mRNA表达变化;倒置相差显微镜观察细胞形态学的变化;间接免疫荧光观察E-cad蛋白表达的变化。结果:倒置相差显微镜观察到TGF-β1干预后A549细胞由鹅卵石状变为梭形,形态如同肌纤维母细胞。间接免疫荧光显示A549细胞的E-cad表达(红色荧光染色)随时间延长逐渐减少。RT-PCR显示E-cad的mRNA表达下调(P<0.05)。结论:TGF-β1在体外诱导肺泡上皮细胞向间质细胞转化,肺泡上皮细胞间质转化是肺纤维化的重要发病机制之一。Objective By observing the cellular morphology changes and the expression of E-cad after A549 cells were treated with transforming growth factorβ1 ( TGF-β1 ) ,to investigate the role of epithelial-mesenchymal transition ( EMT) in the pathogenesy of pulmonary fibrosis.Method A549 cells cultured in vitro were treated by TGF-β1 ,then harvested at different time points to assay mRNA expression of E-cad by real-time PCR ( RT-PCR) before and after A549 cells being treated by TGF-β1.Cellular morphology changes were observed by phase-contrast microscope.Protein expression of E-cad by indirect immunofluorescence.Results After being treated by TGF-β1 ,A549 cells were observed by inverted phase contrast microscope to turn from pebble shape to fusiform shape,a myofibroblast-like morphology.Indirect immunofluorescence showed protein expression of E-cad reduced as time went by( red stain) .The mRNA expression of E-cad was down-regulated in RT-PCR( P 0.05) .Conclusion TGF-β1 induced EMT of alveolar epithelial cells in vitro suggests that EMT of alveolar epithelial cells might be one of fundamental mechanisms of pulmonary fibrosis.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:3.138.174.90