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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本的体外分析。

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.

机构信息

Department of Medical Microbiology, Lokman Hekim University, Faculty of Medicine, Turkey.

Department of Biochemistry, Hacettepe University, Faculty of Pharmacy, Turkey.

出版信息

J Renin Angiotensin Aldosterone Syst. 2020 Apr-Jun;21(2):1470320320928872. doi: 10.1177/1470320320928872.

DOI:10.1177/1470320320928872
PMID:32490715
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7271679/
Abstract

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.

摘要

简介

严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)是一种最近被发现的冠状病毒家族成员,它引发的呼吸道疾病与严重急性呼吸系统综合征冠状病毒(SARS-CoV)相似。SARS-CoV 和 SARS-CoV-2 在许多方面非常相似,例如结构、遗传学和病理生物学。我们假设冠状病毒在与肾素-血管紧张素系统(RAS)元件相互作用后,通过与关键免疫基因整合,可能会影响肺部组织。本生物信息学研究的目的是评估 SARS-CoV 感染后肺上皮细胞中 RAS 和非 RAS 基因(特别是免疫反应基因)的表达变化。

方法

使用 E-GEOD-17400 数据集进行线性回归、层次聚类、途径分析和网络分析。

结果

分析了 SARS-CoV 感染肺上皮细胞 12、24 和 48 小时的全基因组表达数据,总共发现 15 个 RAS 家族和 29 个免疫基因与研究组中暴露于病毒的时间高度相关。

结论

RAS 基因在冠状病毒家族成员引起的感染起始时很重要,并且可能在感染后与免疫基因的交换具有很强的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/498d9ba005c7/10.1177_1470320320928872-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/c9434553a910/10.1177_1470320320928872-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/baba7c74f51d/10.1177_1470320320928872-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/9f45626b0d41/10.1177_1470320320928872-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/ee1194050720/10.1177_1470320320928872-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/498d9ba005c7/10.1177_1470320320928872-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/c9434553a910/10.1177_1470320320928872-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/baba7c74f51d/10.1177_1470320320928872-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/9f45626b0d41/10.1177_1470320320928872-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/ee1194050720/10.1177_1470320320928872-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f854/7271679/498d9ba005c7/10.1177_1470320320928872-fig5.jpg

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