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In vitro analysis of the renin–angiotensin system and inflammatory gene transcripts in human bronchial epithelial cells after infection with severe acute respiratory syndrome coronavirus

机译:对严重急性呼吸综合征冠状病毒感染后人支气管上皮细胞肾素 - 血管紧张素系统和炎症基因转录物的体外分析

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Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a recently identified coronavirus family member that triggers a respiratory disease similar to severe acute respiratory syndrome coronavirus (SARS-CoV). SARS-CoV and SARS-CoV-2 are very similar to each other in many respects, such as structure, genetics, and pathobiology. We hypothesized that coronaviruses could affect pulmonary tissues via integration with the critical immune genes after their interaction with renin–angiotensin system (RAS) elements. The aim of the present bioinformatics study was to assess expression changes of the RAS and non-RAS genes, particularly immune response genes, in the lung epithelial cells after infection with SARS-CoV. Methods: Linear regression, hierarchical clustering, pathway analysis, and network analysis were performed using the E-GEOD-17400 data set. Results: The whole-genome expression data of the lung epithelial cells infected with SARS-CoV for 12, 24, and 48 hours were analyzed, and a total of 15 RAS family and 29 immune genes were found to be highly correlated with the exposure time to the virus in the studied groups. Conclusion: RAS genes are important at the initiation of the infections caused by coronavirus family members and may have a strong relationship with the exchange of immune genes in due course following the infection.
机译:简介:严重急性呼吸综合征冠状病毒2(SARS-COV-2)是最近鉴定的冠状病毒家族成员,触发了类似于严重急性呼吸综合征冠状病毒(SARS-COV)的呼吸系统疾病。 SARS-COV和SARS-COV-2在许多方面彼此非常相似,例如结构,遗传学和病理学。我们假设冠状病毒通过与肾素 - 血管紧张素系统(RAS)元素相互作用后,通过与临界免疫基因的整合来影响肺组织。目前的生物信息学研究的目的是在用SARS-COV感染后评估肺上皮细胞中RAS和非RAS基因,特别是免疫应答基因的表达变化。方法:使用E-GeoD-17400数据集进行线性回归,分层聚类,路径分析和网络分析。结果:分析了用SARS-COV感染12,24和48小时的肺上皮细胞的全基因组表达数据,并发现共15个RAS系列和29个免疫基因与暴露时间高度相关在研究的群体中的病毒。结论:RAS基因在冠状病毒家庭成员引起的感染中是重要的,并且可能与在感染后适当的过程中的免疫基因交换有良好的关系。

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