H7N9流感病毒感染A549细胞蛋白质组学的初步研究
发布时间：2018-09-04 07:51
【摘要】：通过建立H7N9和H1N1流感病毒(H1N1pdm09)感染人肺癌上皮细胞(A549)模型,研究病毒感染细胞后细胞蛋白质组学差异变化,探讨H7N9流感病毒感染人类致病机制。将感染复数(MOI)为0.001的H7N9、H1N1pdm09流感病毒感染A549细胞24h、48h、72h后提取细胞总蛋白进行荧光双向差异凝胶电泳(2D-DIGE)和基质辅助激光解析串联飞行时间质谱(MALDI-TOF-MS/MS)分析鉴定差异蛋白。质谱共鉴定出H7N9和H1N1pdm09流感病毒感染A549细胞24h、48h、72h上调或下调的差异蛋白分别为11、12、33个。对差异蛋白进行功能分析发现与H1N1pdm09感染组相比,(纤)丝状肌动蛋白成帽蛋白α1(F-actin-capping protein subunit alpha-1,CapZ-α1)、鸟氨酸氨基转移酶(Ornithine aminotransferase,OAT)、Poly(rC)-binding protein 1(PCBP1)、真核翻译起始因子5A-1(Eukaryotic translation initiation factor 5A-1,eIF5A)在H7N9感染A549细胞后表达量的下调加速了致细胞病变效应。血小板活化因子乙酰水解酶Ⅰb亚基β(Platelet-activating factor acetylhydrolaseIb subunit beta,PAFAH1B2)在H7N9感染A549细胞后期表达量显著降低可能与该病毒感染患者的临床症状相关。
[Abstract]:By establishing the model of H7N9 and H1N1 influenza virus (H1N1pdm09) infecting human lung cancer epithelial cells (A549), we studied the proteomic changes of cells infected with H7N9 influenza virus, and discussed the pathogenesis of H7N9 influenza virus infection. The total protein was extracted from A549 cells infected with H7N9H1pdm09 influenza virus with a complex (MOI) of 0.001 for 24 h or 48 h and analyzed by fluorescence two dimensional differential gel electrophoresis (2D-DIGE) and matrix assisted laser desorption tandem time-of-flight mass spectrometry (MALDI-TOF-MS/MS). The up-regulated or down-regulated proteins of H7N9 and H1N1pdm09 influenza virus infected A549 cells for 24 h and 48 h / 72 h were 1112,33 respectively. Functional analysis of differentially expressed proteins revealed that filamentous actin cap protein 伪 1 (F-actin-capping protein subunit alpha-1,CapZ- 伪 1), ornithine aminotransferase (Ornithine aminotransferase,OAT) Poly (rC) binding protein 1 (PCBP1) and eukaryotic translation initiation factor 5A-1 (Eukaryotic translation initiation factor 5A-1e IF5A were infected with A549 cells after H7N9 infection. The down-regulation of expression accelerates the cytopathic effect. The decreased expression of platelet activating factor acetylhydrolase 鈪，
本文编号：2221455
[Abstract]:By establishing the model of H7N9 and H1N1 influenza virus (H1N1pdm09) infecting human lung cancer epithelial cells (A549), we studied the proteomic changes of cells infected with H7N9 influenza virus, and discussed the pathogenesis of H7N9 influenza virus infection. The total protein was extracted from A549 cells infected with H7N9H1pdm09 influenza virus with a complex (MOI) of 0.001 for 24 h or 48 h and analyzed by fluorescence two dimensional differential gel electrophoresis (2D-DIGE) and matrix assisted laser desorption tandem time-of-flight mass spectrometry (MALDI-TOF-MS/MS). The up-regulated or down-regulated proteins of H7N9 and H1N1pdm09 influenza virus infected A549 cells for 24 h and 48 h / 72 h were 1112,33 respectively. Functional analysis of differentially expressed proteins revealed that filamentous actin cap protein 伪 1 (F-actin-capping protein subunit alpha-1,CapZ- 伪 1), ornithine aminotransferase (Ornithine aminotransferase,OAT) Poly (rC) binding protein 1 (PCBP1) and eukaryotic translation initiation factor 5A-1 (Eukaryotic translation initiation factor 5A-1e IF5A were infected with A549 cells after H7N9 infection. The down-regulation of expression accelerates the cytopathic effect. The decreased expression of platelet activating factor acetylhydrolase 鈪，
本文编号：2221455
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