首页> 外文期刊>International journal of molecular medicine >Knockdown of long non?coding RNA DLEU2 suppresses idiopathic pulmonary fibrosis by regulating the microRNA?369?3p/TRIM2 axis
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Knockdown of long non?coding RNA DLEU2 suppresses idiopathic pulmonary fibrosis by regulating the microRNA?369?3p/TRIM2 axis

机译:长非敲击性RNA DLE2通过调节MicroRNA抑制特发性肺纤维化,369?3P / Trim2轴抑制特发性肺纤维化

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Idiopathic pulmonary fibrosis (IPF) is the most common form of idiopathic interstitial pneumonia with an increasing incidence. In the present study, Genome Expression Omnibus (GEO) datasets (GSE10667, GSE24206 and GSE32537) were applied to identify lncRNA DLEU2 in IPF. Through prediction using starBase, TargetScan, miRTarBase and miRDB, tripartite motif containing?2?(TRIM2) and prostaglandin F2 receptor inhibitor?(PTGFRN) were found to be upregulated in IPF. DLEU2 expression, the mRNA expression of TRIM2 and PTGFRN, and miR?369?3p expression in A549 cells and lung tissues were detected by RT?qPCR. The protein expression of TRIM2 and PTGFRN in lung tissues and A549 cells was detected by western blot analysis. The proliferation and migration of A549 cells was respectively detected by CCK?8 assay and wound healing assay. The expression of collagen I, α?smooth muscle actin (SMA) and E?cadherin was detected by immunofluorescence assay in A549 cells, and collagen I expression was detected by immunohistochemistry assay in lung tissues. The expression of collagen I, α?SMA and E?cadherin was also detected by western blot analysis in A549 cells and lung tissues.
机译:特发性肺纤维化(IPF)是具有越来越多的发作性的特发性肺炎的形式。在本研究中,应用基因组表达综合组(Geo)数据集(GSE10667,GSE24206和GSE32537)以鉴定IPF中的LNCRNA DLE2。通过使用星巴酶,靶谱,MIRRARBase和MIRDB的预测,发现含有α2?(TRIM2)和前列腺素F2受体抑制剂的三方基序?(PTGFRN)在IPF中上调。 DLEU2表达,TRIM2和PTGFRN的mRNA表达,和miR?369?369?369α在A549细胞和肺组织中的表达检测到RTαQPCR。通过Western印迹分析检测肺组织和A549细胞中TRIM2和PTGFRN的蛋白质表达。通过CCKβ8测定和伤口愈合测定分别检测A549细胞的增殖和迁移。胶原蛋白I,α的表达式α?平滑肌肌动蛋白(SMA)和E?钙粘蛋白被A549细胞中的免疫荧光测定检测,并且通过免疫组织化学测定在肺组织中检测胶原蛋白。在A549细胞和肺组织中,还通过Western印迹分析检测胶原蛋白I,αα和e≥Cadherin的表达。

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