JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells.
Identifieur interne : 000F74 ( Ncbi/Checkpoint ); précédent : 000F73; suivant : 000F75JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells.
Auteurs : Tetsuya Mizutani [Japon] ; Shuetsu Fukushi ; Masayuki Saijo ; Ichiro Kurane ; Shigeru MorikawaSource :
- Biochimica et biophysica acta [ 0006-3002 ] ; 2005.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- Animals, Chlorocebus aethiops, JNK Mitogen-Activated Protein Kinases (metabolism), Phosphatidylinositol 3-Kinases (metabolism), Protein-Serine-Threonine Kinases (metabolism), Proto-Oncogene Proteins (metabolism), Proto-Oncogene Proteins c-akt, SARS Virus (pathogenicity), Signal Transduction, Vero Cells.
- MESH :
- chemical , metabolism : JNK Mitogen-Activated Protein Kinases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins.
- metabolism : Phosphatidylinositol 3-Kinases.
- pathogenicity : SARS Virus.
- Animals, Chlorocebus aethiops, Proto-Oncogene Proteins c-akt, Signal Transduction, Vero Cells.
Abstract
Persistence was established after most of the SARS-CoV-infected Vero E6 cells died. RNA of the defective interfering virus was not observed in the persistently infected cells by Northern blot analysis. SARS-CoV diluted to 2 PFU failed to establish persistence, suggesting that some particular viruses in the seed virus did not induce persistent infection. Interestingly, a viral receptor, angiotensin converting enzyme (ACE)-2, was down-regulated in persistently infected cells. G418-selected clones established from parent Vero E6 cells, which were transfected with a plasmid containing the neomycin resistance gene, were infected with SARS-CoV, resulting in a potential cell population capable of persistence in Vero E6 cells. Our previous studies demonstrated that signaling pathways of extracellular signal-related kinase (ERK1/2), c-Jun N-terminal protein kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3'-kinase (PI3K)/Akt were activated in SARS-CoV-infected Vero E6 cells. Previous studies also showed that the activation of p38 MAPK by viral infection-induced apoptosis, and a weak activation of Akt was not sufficient to protect from apoptosis. In the present study, we showed that the inhibitors of JNK and PI3K/Akt inhibited the establishment of persistence, but those of MAPK/ERK kinase (MEK; as an inhibitor for ERK1/2) and p38 MAPK did not. These results indicated that two signaling pathways of JNK and PI3K/Akt were important for the establishment of persistence in Vero E6 cells.
DOI: 10.1016/j.bbadis.2005.04.004
PubMed: 15916886
Affiliations:
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last="Fukushi">Shuetsu Fukushi</name></author><author><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name></author><author><name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name></author><author><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15916886</idno><idno type="pmid">15916886</idno><idno type="doi">10.1016/j.bbadis.2005.04.004</idno><idno type="wicri:Area/PubMed/Corpus">002716</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002716</idno><idno type="wicri:Area/PubMed/Curation">002716</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002716</idno><idno 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Diseases, Musashimurayama, Tokyo 208-0011</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Fukushi, Shuetsu" sort="Fukushi, Shuetsu" uniqKey="Fukushi S" first="Shuetsu" last="Fukushi">Shuetsu Fukushi</name></author><author><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name></author><author><name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name></author><author><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name></author></analytic><series><title level="j">Biochimica et biophysica acta</title><idno type="ISSN">0006-3002</idno><imprint><date when="2005" 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(pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>JNK Mitogen-Activated Protein Kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Proto-Oncogene Proteins</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>JNK Mitogen-Activated Protein Kinases</term><term>Phosphatidylinositol 3-kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Protéines proto-oncogènes</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chlorocebus aethiops</term><term>Proto-Oncogene Proteins c-akt</term><term>Signal Transduction</term><term>Vero Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules Vero</term><term>Protéines proto-oncogènes c-akt</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Persistence was established after most of the SARS-CoV-infected Vero E6 cells died. RNA of the defective interfering virus was not observed in the persistently infected cells by Northern blot analysis. SARS-CoV diluted to 2 PFU failed to establish persistence, suggesting that some particular viruses in the seed virus did not induce persistent infection. Interestingly, a viral receptor, angiotensin converting enzyme (ACE)-2, was down-regulated in persistently infected cells. G418-selected clones established from parent Vero E6 cells, which were transfected with a plasmid containing the neomycin resistance gene, were infected with SARS-CoV, resulting in a potential cell population capable of persistence in Vero E6 cells. Our previous studies demonstrated that signaling pathways of extracellular signal-related kinase (ERK1/2), c-Jun N-terminal protein kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3'-kinase (PI3K)/Akt were activated in SARS-CoV-infected Vero E6 cells. Previous studies also showed that the activation of p38 MAPK by viral infection-induced apoptosis, and a weak activation of Akt was not sufficient to protect from apoptosis. In the present study, we showed that the inhibitors of JNK and PI3K/Akt inhibited the establishment of persistence, but those of MAPK/ERK kinase (MEK; as an inhibitor for ERK1/2) and p38 MAPK did not. These results indicated that two signaling pathways of JNK and PI3K/Akt were important for the establishment of persistence in Vero E6 cells.</div></front></TEI><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement></list><tree><noCountry><name sortKey="Fukushi, Shuetsu" sort="Fukushi, Shuetsu" uniqKey="Fukushi S" first="Shuetsu" last="Fukushi">Shuetsu Fukushi</name><name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name></noCountry><country name="Japon"><region name="Région de Kantō"><name sortKey="Mizutani, Tetsuya" sort="Mizutani, Tetsuya" uniqKey="Mizutani T" first="Tetsuya" last="Mizutani">Tetsuya Mizutani</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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