Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis
Identifieur interne : 004414 ( Main/Exploration ); précédent : 004413; suivant : 004415Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis
Auteurs : Cheng-Wen Lin [Taïwan] ; Kuan-Hsun Lin [Taïwan] ; Tsung-Han Hsieh [Taïwan] ; Shi-Yi Shiu [Taïwan] ; Jeng-Yi Li [Taïwan]Source :
- FEMS immunology and medical microbiology [ 0928-8244 ] ; 2006.
Descripteurs français
- KwdFr :
- Annexine A5 (), Apoptose (immunologie), Caspase-3, Caspase-9, Caspases (métabolisme), Cysteine endopeptidases (biosynthèse), Cysteine endopeptidases (génétique), Cysteine endopeptidases (immunologie), Espèces réactives de l'oxygène (métabolisme), Facteur de transcription AP-1 (immunologie), Facteur de transcription NF-kappa B (immunologie), Humains, Lignée cellulaire, Microscopie de fluorescence, Protéines virales (biosynthèse), Protéines virales (génétique), Protéines virales (immunologie), Rhodamines (), Syndrome respiratoire aigu sévère (virologie), Transduction du signal, Transfection, Virus du SRAS (enzymologie), Virus du SRAS (génétique), Virus du SRAS (immunologie).
- MESH :
- biosynthèse : Cysteine endopeptidases, Protéines virales.
- enzymologie : Virus du SRAS.
- génétique : Cysteine endopeptidases, Protéines virales, Virus du SRAS.
- immunologie : Apoptose, Cysteine endopeptidases, Facteur de transcription AP-1, Facteur de transcription NF-kappa B, Protéines virales, Virus du SRAS.
- métabolisme : Caspases, Espèces réactives de l'oxygène.
- virologie : Syndrome respiratoire aigu sévère.
- Pascal (Inist)
- Annexine A5, Caspase-3, Caspase-9, Coronavirus, Humains, Lignée cellulaire, Microscopie de fluorescence, Rhodamines, Transduction du signal, Transfection, Virus syndrome respiratoire aigu sévère, Peptidases, Apoptose, Mort cellulaire, Microbiologie, Immunologie, Syndrome respiratoire aigu sévère, Oxygène actif.
- Wicri :
- topic : Immunologie.
English descriptors
- KwdEn :
- Annexin A5 (chemistry), Apoptosis, Apoptosis (immunology), Caspase 3, Caspase 9, Caspases (metabolism), Cell Line, Cell death, Coronavirus, Cysteine Endopeptidases (biosynthesis), Cysteine Endopeptidases (genetics), Cysteine Endopeptidases (immunology), Humans, Immunology, Microbiology, Microscopy, Fluorescence, NF-kappa B (immunology), Peptidases, Reactive Oxygen Species (metabolism), Rhodamines (chemistry), SARS Virus (enzymology), SARS Virus (genetics), SARS Virus (immunology), Severe Acute Respiratory Syndrome (virology), Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Signal Transduction, Transcription Factor AP-1 (immunology), Transfection, Viral Proteins (biosynthesis), Viral Proteins (genetics), Viral Proteins (immunology).
- MESH :
- chemical , biosynthesis : Cysteine Endopeptidases, Viral Proteins.
- chemical , chemistry : Annexin A5, Rhodamines.
- chemical , genetics : Cysteine Endopeptidases, Viral Proteins.
- enzymology : SARS Virus.
- genetics : SARS Virus.
- immunology : Apoptosis, Cysteine Endopeptidases, NF-kappa B, SARS Virus, Transcription Factor AP-1, Viral Proteins.
- chemical , metabolism : Caspases, Reactive Oxygen Species.
- virology : Severe Acute Respiratory Syndrome.
- chemical : Caspase 3, Caspase 9, Cell Line, Humans, Microscopy, Fluorescence, Signal Transduction, Transfection.
Abstract
The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CLpro) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CLpro-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CLpro-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CLpro increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.
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Le document en format XML
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xml:lang="en" level="a">Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis</title><author><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Kuan Hsun" sort="Lin, Kuan Hsun" uniqKey="Lin K" first="Kuan-Hsun" last="Lin">Kuan-Hsun Lin</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Hsieh, Tsung Han" sort="Hsieh, Tsung Han" uniqKey="Hsieh T" first="Tsung-Han" last="Hsieh">Tsung-Han Hsieh</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Shiu, Shi Yi" sort="Shiu, Shi Yi" uniqKey="Shiu S" first="Shi-Yi" last="Shiu">Shi-Yi Shiu</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Li, Jeng Yi" sort="Li, Jeng Yi" uniqKey="Li J" first="Jeng-Yi" last="Li">Jeng-Yi Li</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">FEMS immunology and medical microbiology</title><title level="j" type="abbreviated">FEMS immunol. med. microbiol.</title><idno type="ISSN">0928-8244</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">FEMS immunology and medical microbiology</title><title level="j" type="abbreviated">FEMS immunol. med. microbiol.</title><idno type="ISSN">0928-8244</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Annexin A5 (chemistry)</term><term>Apoptosis</term><term>Apoptosis (immunology)</term><term>Caspase 3</term><term>Caspase 9</term><term>Caspases (metabolism)</term><term>Cell Line</term><term>Cell death</term><term>Coronavirus</term><term>Cysteine Endopeptidases (biosynthesis)</term><term>Cysteine Endopeptidases (genetics)</term><term>Cysteine Endopeptidases (immunology)</term><term>Humans</term><term>Immunology</term><term>Microbiology</term><term>Microscopy, Fluorescence</term><term>NF-kappa B (immunology)</term><term>Peptidases</term><term>Reactive Oxygen Species (metabolism)</term><term>Rhodamines (chemistry)</term><term>SARS Virus (enzymology)</term><term>SARS Virus (genetics)</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Severe acute respiratory syndrome</term><term>Severe acute respiratory syndrome virus</term><term>Signal Transduction</term><term>Transcription Factor AP-1 (immunology)</term><term>Transfection</term><term>Viral Proteins (biosynthesis)</term><term>Viral Proteins (genetics)</term><term>Viral Proteins (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Annexine A5 ()</term><term>Apoptose (immunologie)</term><term>Caspase-3</term><term>Caspase-9</term><term>Caspases (métabolisme)</term><term>Cysteine endopeptidases (biosynthèse)</term><term>Cysteine endopeptidases (génétique)</term><term>Cysteine endopeptidases (immunologie)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Facteur de transcription AP-1 (immunologie)</term><term>Facteur de transcription NF-kappa B (immunologie)</term><term>Humains</term><term>Lignée cellulaire</term><term>Microscopie de fluorescence</term><term>Protéines virales (biosynthèse)</term><term>Protéines virales (génétique)</term><term>Protéines virales (immunologie)</term><term>Rhodamines ()</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Transduction du signal</term><term>Transfection</term><term>Virus du SRAS (enzymologie)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cysteine Endopeptidases</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Annexin A5</term><term>Rhodamines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cysteine Endopeptidases</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Cysteine endopeptidases</term><term>Protéines virales</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cysteine endopeptidases</term><term>Protéines virales</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Apoptose</term><term>Cysteine endopeptidases</term><term>Facteur de transcription AP-1</term><term>Facteur de transcription NF-kappa B</term><term>Protéines virales</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Apoptosis</term><term>Cysteine Endopeptidases</term><term>NF-kappa B</term><term>SARS Virus</term><term>Transcription Factor AP-1</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspases</term><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Caspase 3</term><term>Caspase 9</term><term>Cell Line</term><term>Humans</term><term>Microscopy, Fluorescence</term><term>Signal Transduction</term><term>Transfection</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Annexine A5</term><term>Caspase-3</term><term>Caspase-9</term><term>Coronavirus</term><term>Humains</term><term>Lignée cellulaire</term><term>Microscopie de fluorescence</term><term>Rhodamines</term><term>Transduction du signal</term><term>Transfection</term><term>Virus syndrome respiratoire aigu sévère</term><term>Peptidases</term><term>Apoptose</term><term>Mort cellulaire</term><term>Microbiologie</term><term>Immunologie</term><term>Syndrome respiratoire aigu sévère</term><term>Oxygène actif</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Immunologie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL<sup>pro</sup>) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CL<sup>pro</sup>-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL<sup>pro</sup>-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL<sup>pro</sup> increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name></noRegion><name sortKey="Hsieh, Tsung Han" sort="Hsieh, Tsung Han" uniqKey="Hsieh T" first="Tsung-Han" last="Hsieh">Tsung-Han Hsieh</name><name sortKey="Li, Jeng Yi" sort="Li, Jeng Yi" uniqKey="Li J" first="Jeng-Yi" last="Li">Jeng-Yi Li</name><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><name sortKey="Lin, Kuan Hsun" sort="Lin, Kuan Hsun" uniqKey="Lin K" first="Kuan-Hsun" last="Lin">Kuan-Hsun Lin</name><name sortKey="Shiu, Shi Yi" sort="Shiu, Shi Yi" uniqKey="Shiu S" first="Shi-Yi" last="Shiu">Shi-Yi Shiu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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