Upregulation of the chemokine (C-C motif) ligand 2 via a severe acute respiratory syndrome coronavirus spike-ACE2 signaling pathway.
Identifieur interne : 002411 ( Main/Exploration ); précédent : 002410; suivant : 002412Upregulation of the chemokine (C-C motif) ligand 2 via a severe acute respiratory syndrome coronavirus spike-ACE2 signaling pathway.
Auteurs : I-Yin Chen [Taïwan] ; Shin C. Chang ; Hung-Yi Wu ; Ting-Chun Yu ; Wen-Chin Wei ; Shiming Lin ; Chung-Liang Chien ; Ming-Fu ChangSource :
- Journal of virology [ 1098-5514 ] ; 2010.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Cellules épithéliales (virologie), Chimiokine CCL2 (biosynthèse), Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (immunologie), Humains, Lignée cellulaire, Peptidyl-Dipeptidase A (métabolisme), Protéines de l'enveloppe virale (immunologie), RT-PCR, Régulation positive, Séquençage par oligonucléotides en batterie, Test ELISA, Transduction du signal, Virus du SRAS (immunologie).
- MESH :
- biosynthèse : Chimiokine CCL2.
- immunologie : Glycoprotéines membranaires, Protéines de l'enveloppe virale, Virus du SRAS.
- métabolisme : Peptidyl-Dipeptidase A.
- virologie : Cellules épithéliales.
- Analyse de profil d'expression de gènes, Glycoprotéine de spicule des coronavirus, Humains, Lignée cellulaire, RT-PCR, Régulation positive, Séquençage par oligonucléotides en batterie, Test ELISA, Transduction du signal.
English descriptors
- KwdEn :
- Cell Line, Chemokine CCL2 (biosynthesis), Enzyme-Linked Immunosorbent Assay, Epithelial Cells (virology), Gene Expression Profiling, Humans, Membrane Glycoproteins (immunology), Oligonucleotide Array Sequence Analysis, Peptidyl-Dipeptidase A (metabolism), Reverse Transcriptase Polymerase Chain Reaction, SARS Virus (immunology), Signal Transduction, Spike Glycoprotein, Coronavirus, Up-Regulation, Viral Envelope Proteins (immunology).
- MESH :
- chemical , biosynthesis : Chemokine CCL2.
- chemical , immunology : Membrane Glycoproteins, Viral Envelope Proteins.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- immunology : SARS Virus.
- virology : Epithelial Cells.
- Cell Line, Enzyme-Linked Immunosorbent Assay, Gene Expression Profiling, Humans, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Spike Glycoprotein, Coronavirus, Up-Regulation.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) was identified to be the causative agent of SARS with atypical pneumonia. Angiotensin-converting enzyme 2 (ACE2) is the major receptor for SARS-CoV. It is not clear whether ACE2 conveys signals from the cell surface to the nucleus and regulates expression of cellular genes upon SARS-CoV infection. To understand the pathogenesis of SARS-CoV, human type II pneumocyte (A549) cells were incubated with the viral spike protein or with SARS-CoV virus-like particles containing the viral spike protein to examine cytokine modulation in lung cells. Results from oligonucleotide-based microarray, real-time PCR, and enzyme-linked immunosorbent assays indicated an upregulation of the fibrosis-associated chemokine (C-C motif) ligand 2 (CCL2) by the viral spike protein and the virus-like particles. The upregulation of CCL2 by SARS-CoV spike protein was mainly mediated by extracellular signal-regulated kinase 1 and 2 (ERK1/2) and AP-1 but not the IkappaBalpha-NF-kappaB signaling pathway. In addition, Ras and Raf upstream of the ERK1/2 signaling pathway were involved in the upregulation of CCL2. Furthermore, ACE2 receptor was activated by casein kinase II-mediated phosphorylation in cells pretreated with the virus-like particles containing spike protein. These results indicate that SARS-CoV spike protein triggers ACE2 signaling and activates fibrosis-associated CCL2 expression through the Ras-ERK-AP-1 pathway.
DOI: 10.1128/JVI.02560-09
PubMed: 20484496
Affiliations:
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Chang</name></author><author><name sortKey="Wu, Hung Yi" sort="Wu, Hung Yi" uniqKey="Wu H" first="Hung-Yi" last="Wu">Hung-Yi Wu</name></author><author><name sortKey="Yu, Ting Chun" sort="Yu, Ting Chun" uniqKey="Yu T" first="Ting-Chun" last="Yu">Ting-Chun Yu</name></author><author><name sortKey="Wei, Wen Chin" sort="Wei, Wen Chin" uniqKey="Wei W" first="Wen-Chin" last="Wei">Wen-Chin Wei</name></author><author><name sortKey="Lin, Shiming" sort="Lin, Shiming" uniqKey="Lin S" first="Shiming" last="Lin">Shiming Lin</name></author><author><name sortKey="Chien, Chung Liang" sort="Chien, Chung Liang" uniqKey="Chien C" first="Chung-Liang" last="Chien">Chung-Liang Chien</name></author><author><name sortKey="Chang, Ming Fu" sort="Chang, Ming Fu" uniqKey="Chang M" first="Ming-Fu" last="Chang">Ming-Fu Chang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20484496</idno><idno type="pmid">20484496</idno><idno type="doi">10.1128/JVI.02560-09</idno><idno type="wicri:Area/PubMed/Corpus">001697</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001697</idno><idno type="wicri:Area/PubMed/Curation">001697</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001697</idno><idno type="wicri:Area/PubMed/Checkpoint">001558</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001558</idno><idno type="wicri:Area/Ncbi/Merge">002139</idno><idno type="wicri:Area/Ncbi/Curation">002139</idno><idno type="wicri:Area/Ncbi/Checkpoint">002139</idno><idno type="wicri:Area/Main/Merge">002442</idno><idno type="wicri:Area/Main/Curation">002411</idno><idno type="wicri:Area/Main/Exploration">002411</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Upregulation of the chemokine (C-C motif) ligand 2 via a severe acute respiratory syndrome coronavirus spike-ACE2 signaling pathway.</title><author><name sortKey="Chen, I Yin" sort="Chen, I Yin" uniqKey="Chen I" first="I-Yin" last="Chen">I-Yin Chen</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Biochemistry and Molecular Biology, National Taiwan University College of Medicine, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Biochemistry and Molecular Biology, National Taiwan University College of Medicine, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Chang, Shin C" sort="Chang, Shin C" uniqKey="Chang S" first="Shin C" last="Chang">Shin C. Chang</name></author><author><name sortKey="Wu, Hung Yi" sort="Wu, Hung Yi" uniqKey="Wu H" first="Hung-Yi" last="Wu">Hung-Yi Wu</name></author><author><name sortKey="Yu, Ting Chun" sort="Yu, Ting Chun" uniqKey="Yu T" first="Ting-Chun" last="Yu">Ting-Chun Yu</name></author><author><name sortKey="Wei, Wen Chin" sort="Wei, Wen Chin" uniqKey="Wei W" first="Wen-Chin" last="Wei">Wen-Chin Wei</name></author><author><name sortKey="Lin, Shiming" sort="Lin, Shiming" uniqKey="Lin S" first="Shiming" last="Lin">Shiming Lin</name></author><author><name sortKey="Chien, Chung Liang" sort="Chien, Chung Liang" uniqKey="Chien C" first="Chung-Liang" last="Chien">Chung-Liang Chien</name></author><author><name sortKey="Chang, Ming Fu" sort="Chang, Ming Fu" uniqKey="Chang M" first="Ming-Fu" last="Chang">Ming-Fu Chang</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line</term><term>Chemokine CCL2 (biosynthesis)</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Epithelial Cells (virology)</term><term>Gene Expression Profiling</term><term>Humans</term><term>Membrane Glycoproteins (immunology)</term><term>Oligonucleotide Array Sequence Analysis</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>SARS Virus (immunology)</term><term>Signal Transduction</term><term>Spike Glycoprotein, Coronavirus</term><term>Up-Regulation</term><term>Viral Envelope Proteins (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Cellules épithéliales (virologie)</term><term>Chimiokine CCL2 (biosynthèse)</term><term>Glycoprotéine de spicule des coronavirus</term><term>Glycoprotéines membranaires (immunologie)</term><term>Humains</term><term>Lignée cellulaire</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Protéines de l'enveloppe virale (immunologie)</term><term>RT-PCR</term><term>Régulation positive</term><term>Séquençage par oligonucléotides en batterie</term><term>Test ELISA</term><term>Transduction du signal</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Chemokine CCL2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Membrane Glycoproteins</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Chimiokine CCL2</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Glycoprotéines membranaires</term><term>Protéines de l'enveloppe virale</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Cellules épithéliales</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Gene Expression Profiling</term><term>Humans</term><term>Oligonucleotide Array Sequence Analysis</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Signal Transduction</term><term>Spike Glycoprotein, Coronavirus</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Glycoprotéine de spicule des coronavirus</term><term>Humains</term><term>Lignée cellulaire</term><term>RT-PCR</term><term>Régulation positive</term><term>Séquençage par oligonucléotides en batterie</term><term>Test ELISA</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) was identified to be the causative agent of SARS with atypical pneumonia. Angiotensin-converting enzyme 2 (ACE2) is the major receptor for SARS-CoV. It is not clear whether ACE2 conveys signals from the cell surface to the nucleus and regulates expression of cellular genes upon SARS-CoV infection. To understand the pathogenesis of SARS-CoV, human type II pneumocyte (A549) cells were incubated with the viral spike protein or with SARS-CoV virus-like particles containing the viral spike protein to examine cytokine modulation in lung cells. Results from oligonucleotide-based microarray, real-time PCR, and enzyme-linked immunosorbent assays indicated an upregulation of the fibrosis-associated chemokine (C-C motif) ligand 2 (CCL2) by the viral spike protein and the virus-like particles. The upregulation of CCL2 by SARS-CoV spike protein was mainly mediated by extracellular signal-regulated kinase 1 and 2 (ERK1/2) and AP-1 but not the IkappaBalpha-NF-kappaB signaling pathway. In addition, Ras and Raf upstream of the ERK1/2 signaling pathway were involved in the upregulation of CCL2. Furthermore, ACE2 receptor was activated by casein kinase II-mediated phosphorylation in cells pretreated with the virus-like particles containing spike protein. These results indicate that SARS-CoV spike protein triggers ACE2 signaling and activates fibrosis-associated CCL2 expression through the Ras-ERK-AP-1 pathway.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><noCountry><name sortKey="Chang, Ming Fu" sort="Chang, Ming Fu" uniqKey="Chang M" first="Ming-Fu" last="Chang">Ming-Fu Chang</name><name sortKey="Chang, Shin C" sort="Chang, Shin C" uniqKey="Chang S" first="Shin C" last="Chang">Shin C. Chang</name><name sortKey="Chien, Chung Liang" sort="Chien, Chung Liang" uniqKey="Chien C" first="Chung-Liang" last="Chien">Chung-Liang Chien</name><name sortKey="Lin, Shiming" sort="Lin, Shiming" uniqKey="Lin S" first="Shiming" last="Lin">Shiming Lin</name><name sortKey="Wei, Wen Chin" sort="Wei, Wen Chin" uniqKey="Wei W" first="Wen-Chin" last="Wei">Wen-Chin Wei</name><name sortKey="Wu, Hung Yi" sort="Wu, Hung Yi" uniqKey="Wu H" first="Hung-Yi" last="Wu">Hung-Yi Wu</name><name sortKey="Yu, Ting Chun" sort="Yu, Ting Chun" uniqKey="Yu T" first="Ting-Chun" last="Yu">Ting-Chun Yu</name></noCountry><country name="Taïwan"><noRegion><name sortKey="Chen, I Yin" sort="Chen, I Yin" uniqKey="Chen I" first="I-Yin" last="Chen">I-Yin Chen</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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