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M and N proteins of SARS coronavirus induce apoptosis in HPF cells

机译:SARS冠状病毒的M和N蛋白诱导HPF细胞凋亡

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Background: SARS-associated coronavirus (SARS-CoV) induced cell apoptosis and its structural proteins may play a role in this process. Objectives: To determine whether the structural proteins M and N of SARS-CoV induce apoptosis. Study design: We investigated human pulmonary fibroblast (HPF) cells, were transfected with plasmids containing the M or N gene, by TdT-mediated dUTP nick end labeling (TUNEL), Hoechst 33342 staining for nuclei, and observation of morphology. Results: We found that in the absence of serum about 16.34% of cells transfected by pcDNA3.1-M and 21.72% of N-transfected cells showed typical apoptotic characteristics, significantly different from mock-transfected cells (only 6.23%, p<0.01). Furthermore, the cells that were co-transfected with M and N proteins showed more obvious phenomena of cell death (about 36.03%). There was a statistical significance between M-transfected cells and co-transfected cells (p<0.01), and a remarkable difference between N-transfected cells and co-transfected cells (p<0.01). Conclusions: The results show that M and N proteins of SARS-CoV can induce apoptosis of HPF cells. Co-transfection of M and N enhances the induction of apoptosis by M or N alone, which also suggests that the structural proteins of SARS-CoV may play an important role not only in the process of invasion but also in the pathogenetic process in cells.
机译:背景:SARS相关冠状病毒(SARS-CoV)诱导细胞凋亡,其结构蛋白可能在此过程中起作用。目的:确定SARS-CoV的结构蛋白M和N是否诱导细胞凋亡。研究设计:我们研究了人类肺成纤维细胞(HPF),并通过TdT介导的dUTP缺口末端标记(TUNEL),Hoechst 33342核染色以及形态学观察,用含有M或N基因的质粒转染。结果:我们发现在无血清的情况下,约有16.34%的pcDNA3.1-M转染的细胞和21.72%的N转染的细胞表现出典型的凋亡特征,与模拟转染的细胞明显不同(仅6.23%,p <0.01 )。此外,用M和N蛋白共转染的细胞表现出更明显的细胞死亡现象(约36.03%)。 M转染的细胞和共转染的细胞之间具有统计学意义(p <0.01),而N转染的细胞和共转染的细胞之间具有显着差异(p <0.01)。结论:SARS-CoV的M和N蛋白可诱导HPF细胞凋亡。 M和N的共转染增强了单独M或N诱导的凋亡,这也表明SARS-CoV的结构蛋白不仅在侵袭过程中而且在细胞的致病过程中都可能起重要作用。

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