Correlation between <scp>TGF</scp>‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease

Li, Shih Wen; Yang, Tsuey Ching; Wan, Lei; Lin, Ying; Tsai, Fuu Jen; Lai, Chien‐Chen; Lin, Cheng Wen

doi:10.1002/pmic.201200225

Cited by 26 publications

(41 citation statements)

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“…Human alveolar basal epithelial A549 cells grew in Dulbecco's Modified Eagle's Medium (HyClone Laboratories) and were transfected with control vector pcDNA3.1/His C (Invitrogen), or pSARS-PLpro containing SARS-CoV PLpro gene, as described in our prior reports (Li et al, 2011(Li et al, , 2012(Li et al, , 2016a(Li et al, , 2016b. In addition, pSARS-PLpro (H273A) that had the alanine substitution for histidine at position 273 by Ala within PLpro gene was constructed using PCR-based sitedirected mutagenesis with a mutated primer pair (5′-GGTAACT ATC-AGTGTGGTGCTTACACTCATATAACTGCTAAG-3′ and 5′-CTTAGCAGT TATATGAGTGTAAGCACCACACTGATAGTTACC-3′).…”

Section: Cell Culture and Transient Transfectionmentioning

confidence: 99%

“…The peptides of ubiquitin-conjugated proteins were recovered for NanoLC-MS/MS spectra. Proteins were identified according to mass spectra obtained were compared to SwissPort database (release 51.0) via MASCOT algorithm (version 2.2.07), as described in our prior reports (Li et al, 2012). Peptides were identified if MASCOT individual ion scores exceeded 30.…”

Section: Identification Of Ubiquitin-conjugated Proteins Nanolc-ms/msmentioning

confidence: 99%

“…PLpro has been demonstrated to trigger the TGF-β1 production in human promonocytes, human lung epithelial cells, and pulmonary tissues in mouse models (Li et al, 2012(Li et al, , 2016b. SARS-CoV PLpro induced the ROS-mediated p38 MAPK and STAT3 activation of Egr-1 expression, in which Egr-1 specifically bound to the TGF-β1 promoter region between −175 to −60, resulting in the increase of TGF-β1 production.…”

Section: Sars-covmentioning

confidence: 99%

“…SARS-CoV up-regulates pro-inflammatory cytokines like IFN-γ, IL-18, TGF-β1, TNF-α, IL-6, IP-10, MCP-1, MIG, and IL-8 (Huang et al, 2005;He et al, 2006), in which recruits immune responder cells into the lungs, triggers acute respiratory distress syndrome (ARDS), and even causes lung fibrosis in the late phase (Huang et al, 2005;He et al, 2006). Among SARS-CoV proteins, the nucleocapsid induces a Smad3dependent induction of TGF-β1 expression (Zhao et al, 2008); spike protein stimulates the IL-8 up-regulation in lung cells (Chang et al, 2004); NSP1 provokes the expression of CCL5, CXVL10, and CCL3 (Law et al, 2007); PLpro elavates the production of TGF-β1 and pro-fibrotic markers via ubiquitin proteasome, p38 MAPK, and ERK1/2-mediated signaling (Li et al, 2012). Recently, SARS-CoV PLpro notably initiates ROS/p38 MAPK/STAT3 pathway to activate Egr-1 dependent expression of TSP-1, TGF-β1 and vimentin in vitro and in vivo (Li et al, 2016b).…”

Section: Introductionmentioning

confidence: 99%

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

Wang

et al. 2017

Virus Research

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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.

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Section: Cell Culture and Transient Transfectionmentioning

confidence: 99%

Section: Identification Of Ubiquitin-conjugated Proteins Nanolc-ms/msmentioning

confidence: 99%

Section: Sars-covmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Wang

et al. 2017

Virus Research

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“…By the time the outbreak had been contained, over 8000 cases had been confirmed and 916 people had died due to the disease [40e45]. According to the World Health Organization, the mortality rate associated with SARS was >10% [46,47]. People of advanced age were at the greatest risk of death, with a case-fatality rate approaching 50% in people >65 years who were infected by the virus [48].…”

mentioning

confidence: 99%

Human coronaviruses: Clinical features and phylogenetic analysis

Lin

2013

BioMedicine

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Keywords: human betacoronavirus 2c EMC2012 human coronavirus phylogenetic tree severe acute respiratory syndrome coronavirus (SARS-CoV) a b s t r a c t Strains of human coronavirus (HCoV), namely HCoV-OC43, HCoV-229E, HCoV-NL63, and HCoV-HKU1, primarily infect the upper respiratory and gastrointestinal tracts and are the most common cause of non-rhinovirus-induced common cold in humans. Although the manifestations of coronavirus infection (i.e., rhinorrhea, sneezing, cough, nasal obstruction, and bronchitis) are generally self-limiting in healthy adults, certain strains such as HCoV-NL63 and HCoV-HKU1 can cause severe lower respiratory tract infection and febrile seizure, especially in infants, people of advanced age, and immunocompromised hosts. In 2003, a novel HCoV strain was identified as the causative agent of the severe acute respiratory syndrome (SARS) epidemic that began in Asia in 2002. The strain has hence been referred to as SARS-CoV. In addition, as recently as September 2012, another novel HCoV, human betacoronavirus 2c EMC2012, was identified as being the cause of fever, renal failure, pneumonia, and severe respiratory distress in two patients in the Middle East.Phylogenetic analysis has revealed highly conserved sequences of ORF1ab, spike, nucleocapsid, and envelope protein genes, but not membrane protein genes, between human betacoronavirus 2c EMC2012 and SARS-CoV. This review focuses on the differences in the genomes of certain HCoV strains, the pathogenesis of said strains, and recent developments in the establishment of therapeutic agents that might aid in the treatment of patients with such infections.

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Targeting SARS‐CoV‐2 viral proteases as a therapeutic strategy to treat COVID‐19

Anirudhan

Lee

Cheng

et al. 2021

Journal of Medical Virology

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The 21st century has witnessed three outbreaks of coronavirus (CoVs) infections caused by severe acute respiratory syndrome (SARS)-CoV, Middle East respiratory syndrome (MERS)-CoV, and SARS-CoV-2. Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, spreads rapidly and since the discovery of the first COVID-19 infection in December 2019, has caused 1.2 million deaths worldwide and 226,777 deaths in the United States alone. The high amino acid similarity between SARS-CoV and SARS-CoV-2 viral proteins supports testing therapeutic molecules that were designed to treat SARS infections during the 2003 epidemic. In this review, we provide information on possible COVID-19 treatment strategies that act via inhibition of the two essential proteins of the virus, 3C-like protease (3CL pro ) or papain-like protease (PL pro ). K E Y W O R D S 3 chymotrypsin-like cysteine protease, coronavirus main protease, COVID-19, papain-like cysteine protease, SARS coronavirus, SARS-CoV-2 1 | INTRODUCTION Coronaviruses (CoVs) belong to the Nidovirales order of enveloped positive-sense single-stranded RNA viruses. Before 2002, there were only two known human CoV species, HCoV-229E and HCoV-OC43, with infections exhibiting symptoms similar to those of the common cold caused by rhinovirus. These two CoV were identified in 1965 and have been extensively studied for the following 20 years. 1 There are now seven known species of human CoVs (HCoVs): HCoV-229E, HCoV-OC43, HCoV-NL63, HCoV-HKU1, MERS-CoV, SARS-CoV, and SARS-CoV-2 belonging to alpha-and beta-coronaviruses (Figure 1A). 2 About 30% of mild upper respiratory diseases are caused by HCoV-229E, HCoV-OC43, HCoV-NL63, and HCoV-HKU1. 3,4 SARS-CoV and MERS-CoV, which first appeared in China in 2002 and in Saudi Arabia in 2012, respectively, caused severe health and economic crisis at the global level. Even though its infection rate is slow, MERS-CoV infections are still ongoing and between January 2020 and September 2020, 61 new cases were reported with 21 deaths. The mortality rate of MERS ( 30%) is about three times more than that of SARS (10%).The recently emerged novel SARS-CoV-2, which is currently wreaking havoc worldwide, has infected 44 million individuals and caused 1.2 million deaths as of November 10, 2020 (https:// coronavirus.jhu.edu/map.html). SARS-CoV-2 infection results in coronavirus disease 2019 and the clinical manifestations include fever (88.7%), dry cough (67.8%), sore throat (13.9%), dyspnea (18.6%), fatigue (38.1%) and gastrointestinal symptoms (8.8%). SARS-CoV-2 is a close cousin of SARS-CoV, sharing an overall amino-acid sequence identity of 82%. 5 Based on this similarity it is reasonable to assume that knowledge of the molecular pathogenesis of SARS-CoV could help develop SARS-CoV-2 treatment strategies. Currently, the US FDA has approved remdesivir

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Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease

Cited by 26 publications

References 41 publications

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

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

Human coronaviruses: Clinical features and phylogenetic analysis

Targeting SARS‐CoV‐2 viral proteases as a therapeutic strategy to treat COVID‐19

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