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自噬和未折叠蛋白反应的诱导:街头狂犬病毒与宿主之间的串扰。

Autophagy and unfolded protein response induction: a crosstalk between street rabies virus and the host.

机构信息

Department of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, Iran.

Department of Epidemiology and Biostatistics, Pasteur Institute of Iran, Tehran, Iran.

出版信息

Cell Stress Chaperones. 2023 Jul;28(4):423-428. doi: 10.1007/s12192-023-01335-y. Epub 2023 May 3.

Abstract

The endoplasmic reticulum (ER) response mechanism to cellular stress is mediated by the unfolded protein response/ER-associated degradation (UPR/ERAD) pathway. A viral infection can trigger ER stress and engage some transcription factors, depending on the host cell and virus type, activating or inhibiting autophagy. The relationship between ER response and autophagy in rabies has not been investigated yet. In the present study, the mouse brain was infected with street rabies virus (SRABV). Total RNA was extracted from the brains of animals, and cDNA was synthesized. Next, real-time PCR assay was performed using specific primers. The expression of hypoxanthine-guanine phosphoribosyltransferase (Hprt), CCAAT/enhancer binding protein homologous protein (CHOP), apoptosis signal-regulating kinase 1 (ASK1), activating transcription factor 6 (ATF6), and caspase 3 (CASP3) genes was also investigated. Based on the results, SRABV caused significant changes in the mRNA expression of ATF6, CHOP, and ASK1 genes in the brains of infected mice in the control group (group V). Treatment of infected cells with the pIRES-EGFP-Beclin-1 vector and rapamycin caused changes in nearly most of the parameters. However, alterations in CASP3 gene expression were only observed when the vector and the virus were simultaneously injected into the cells. Overall, protection and autophagy against cell death induced by SRABV infection can be achieved by activating the ER stress pathway, followed by a marked increase in the expression of ATF6, CHOP, ASK1, and CASP3 genes.

摘要

内质网(ER)对细胞应激的反应机制是通过未折叠蛋白反应/ER 相关降解(UPR/ERAD)途径介导的。病毒感染可以触发 ER 应激,并根据宿主细胞和病毒类型,激活或抑制自噬。狂犬病中 ER 反应与自噬之间的关系尚未被研究。在本研究中,用街毒狂犬病病毒(SRABV)感染小鼠大脑。从动物大脑中提取总 RNA,并合成 cDNA。接下来,使用特异性引物进行实时 PCR 检测。还研究了 hypoxanthine-guanine phosphoribosyltransferase (Hprt)、CCAAT/enhancer binding protein homologous protein (CHOP)、apoptosis signal-regulating kinase 1 (ASK1)、activating transcription factor 6 (ATF6) 和 caspase 3 (CASP3) 基因的表达。基于结果,SRABV 导致对照组(V 组)感染小鼠大脑中 ATF6、CHOP 和 ASK1 基因的 mRNA 表达发生显著变化。用 pIRES-EGFP-Beclin-1 载体和雷帕霉素处理感染细胞导致几乎大多数参数发生变化。然而,只有当载体和病毒同时注入细胞时,CASP3 基因的表达才发生改变。总的来说,通过激活 ER 应激途径,可以实现对 SRABV 感染诱导的细胞死亡的保护和自噬,随后 ATF6、CHOP、ASK1 和 CASP3 基因的表达明显增加。

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