ER stress-related molecules induced by Hantaan virus infection in differentiated THP-1 cells
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ORIGINAL PAPER
ER stress-related molecules induced by Hantaan virus infection in differentiated THP-1 cells Zhuo Li 1,2 & Yuting Shen 1 & Yun Song 1 & Yusi Zhang 1 & Chunmei Zhang 1 & Ying Ma 1 & Fanglin Zhang 3 & Lihua Chen 1 Received: 16 May 2020 / Revised: 30 July 2020 / Accepted: 6 August 2020 # Cell Stress Society International 2020
Abstract Endoplasmic reticulum stress (ER stress) can be induced by virus infection. In this part, we explored whether Hantaan virus (HTNV) infection could induce ER stress in differentiated THP-1 (dTHP-1) cells. It showed that the mRNA and protein levels of ER stress-related 78 kDa glucose-regulated protein (GRP78, HSPA5) and mRNA levels of X box-binding protein 1 (XBP-1), activating transcription factor 6(ATF6) and PKR-like ER kinase (PERK) after HTNV infection, were significantly higher than that in uninfected control group. However, the mRNA levels of C/EBP homologous protein (CHOP), glucose-regulated protein 94 (GRP94, HSPC4), and inositol-requiring enzyme1 (IRE1) were not significantly different between the infected group and the untreated group in 2 h after virus infection. It is unusual in activating GRP78 but not GRP94. Meanwhile, dTHP-1 cells infected with HTNV at 12 h did not show obvious apoptosis. These results indicated that the HTNV infection could induce the unfolded protein response (UPR) in dTHP-1 cells, without directly leading to cell apoptosis during 12 h after virus infection. Keywords Hantaan virus (HTNV) . Hemorrhagic fever with renal syndrome (HFRS) . Endoplasmic reticulum stress (ER stress) . 78 kDa glucose-regulated protein (GRP78, HSPA5) . dTHP-1
Introduction Endoplasmic reticulum stress (ER stress) is the stress response to the accumulation of a large number of unfolded proteins in the endoplasmic reticulum. Cells respond to ER stress through unfolded protein reaction, autophagy, and apoptosis (Mehrbod et al. 2019 ). Previous studies have found that many viruses cause ER stress after they infect cells, such as hepatitis B virus (HBV), hepatitis C virus, human immunodeficiency virus (HIV), rhinovirus, and Newcastle disease virus (Bhoola and Kramvis 2017; Medvedev et al. 2017; Fan and He 2016; Liu et al. 2017; Bu et al. 2016; Sepulveda-Salinas and Ramos-
* Fanglin Zhang [email protected] * Lihua Chen [email protected] 1
Department of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi’an 710032, Shaanxi, China
2
Department of Medical Laboratory Technology, Xi’an Health School, Xi’an, Shaanxi, China
3
Department of Microbiology, The Fourth Military Medical University, Xi’an, Shaanxi, China
Castaneda 2017; Johnston and McCormick 2020). However, due to the different types of viruses, time of infection, and number of cells, the fate of the cells is different. For example, the expression of 78 kDa glucose-regulated protein (GRP78) in HepG2 cells induced by HBV infection inhibited the replication of HBV via the interferon beta1-2',5'-oligoadenylate synthetase-RNase L pathway to balance the stress caused by HBV to protect t
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