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严重急性呼吸综合征冠状病毒木瓜样蛋白酶通过非Smad转化生长因子-β1信号上调胶原蛋白表达。

SARS coronavirus papain-like protease up-regulates the collagen expression through non-Samd TGF-β1 signaling.

作者信息

Wang Ching-Ying, Lu Chien-Yi, Li Shih-Wen, Lai Chien-Chen, Hua Chun-Hung, Huang Su-Hua, Lin Ying-Ju, Hour Mann-Jen, Lin Cheng-Wen

机构信息

Department of Medical Laboratory Science and Biotechnology, China Medical University, Taiwan.

Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan.

出版信息

Virus Res. 2017 May 2;235:58-66. doi: 10.1016/j.virusres.2017.04.008. Epub 2017 Apr 13.

DOI:10.1016/j.virusres.2017.04.008
PMID:28414040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7114548/
Abstract

SARS coronavirus (CoV) papain-like protease (PLpro) reportedly induced the production of TGF-β1 through p38 MAPK/STAT3-meidated Egr-1-dependent activation (Sci. Rep. 6, 25754). This study investigated the correlation of PLpro-induced TGF-β1 with the expression of Type I collagen in human lung epithelial cells and mouse pulmonary tissues. Specific inhibitors for TGF-βRI, p38 MAPK, MEK, and STAT3 proved that SARS-CoV PLpro induced TGF-β1-dependent up-regulation of Type I collagen in vitro and in vivo. Subcellular localization analysis of SMAD3 and SMAD7 indicated that non-SMAD pathways in TGF-β1 signaling involved in the production of Type I collagen in transfected cells with pSARS-PLpro. Comprehensive analysis of ubiquitin-conjugated proteins using immunoprecipitation and nanoLC-MS/MS indicated that SARS-CoV PLpro caused the change in the ubiquitination profile of Rho GTPase family proteins, in which linked with the increase of Rho-like GTPase family proteins. Moreover, selective inhibitors TGF-βRI and STAT6 (AS1517499) ascertained that STAT6 activation was required for PLpro-induced TGF-β1-dependent up-regulation of Type I collagen in human lung epithelial cells. The results showed that SARS-CoV PLpro stimulated TGF-β1-dependent expression of Type I collagen via activating STAT6 pathway.

摘要

据报道，严重急性呼吸综合征冠状病毒（SARS-CoV）木瓜样蛋白酶（PLpro）通过p38丝裂原活化蛋白激酶（MAPK）/信号转导和转录激活因子3（STAT3）介导的早期生长反应因子1（Egr-1）依赖性激活诱导转化生长因子-β1（TGF-β1）的产生（《科学报告》6，25754）。本研究调查了PLpro诱导的TGF-β1与人类肺上皮细胞和小鼠肺组织中I型胶原蛋白表达的相关性。TGF-βRI、p38 MAPK、丝裂原活化蛋白激酶激酶（MEK）和STAT3的特异性抑制剂证明，SARS-CoV PLpro在体外和体内均可诱导TGF-β1依赖性I型胶原蛋白上调。SMAD3和SMAD7的亚细胞定位分析表明，在转染pSARS-PLpro的细胞中，TGF-β1信号传导中的非SMAD途径参与了I型胶原蛋白的产生。使用免疫沉淀和纳升级液相色谱-串联质谱（nanoLC-MS/MS）对泛素共轭蛋白进行的综合分析表明，SARS-CoV PLpro导致Rho鸟苷三磷酸酶（GTPase）家族蛋白的泛素化谱发生变化，其中与Rho样GTPase家族蛋白的增加有关。此外，TGF-βRI和STAT6（AS1517499）的选择性抑制剂确定，STAT6激活是PLpro诱导的人类肺上皮细胞中TGF-β1依赖性I型胶原蛋白上调所必需的。结果表明，SARS-CoV PLpro通过激活STAT6途径刺激TGF-β依赖性I型胶原蛋白的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/6f751de2a719/gr7_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/0fad71c8e7e0/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/ac78f1b24ad2/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/1a2e800e78f7/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/cd39919bc2b8/gr4_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/597a02b10813/gr5_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/7f47174abdaf/gr6_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/6f751de2a719/gr7_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/0fad71c8e7e0/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/ac78f1b24ad2/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/1a2e800e78f7/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/cd39919bc2b8/gr4_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/597a02b10813/gr5_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/7f47174abdaf/gr6_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f99f/7114548/6f751de2a719/gr7_lrg.jpg

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