SrasV1, Main, Exploration, bibRecord, 004438

Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells

Identifieur interne : 004438 ( Main/Exploration ); précédent : 004437; suivant : 004439

Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells

Auteurs : Tetsuya Mizutani [Japon] ; Shuetsu Fukushi [Japon] ; Daisuke Lizuka [Japon] ; Osamu Inanami [Japon] ; Mikinori Kuwabara [Japon] ; Hideaki Takashima [Japon] ; Hiroshi Yanagawa [Japon] ; Masayuki Saijo [Japon] ; Ichiro Kurane [Japon] ; Shigeru Morikawa [Japon]

Source :

FEMS immunology and medical microbiology [ 0928-8244 ] ; 2006.

RBID : Pascal:06-0215620

Descripteurs français

KwdFr :
- Animaux, Apoptose, Cellules Vero, Glycogen Synthase Kinase 3 (génétique), Glycogen Synthase Kinase 3 (métabolisme), Humains, Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Phosphorylation, Prolifération cellulaire, Protéines proto-oncogènes c-akt (génétique), Protéines proto-oncogènes c-akt (métabolisme), Régulation de l'expression des gènes, Transduction du signal, Virus du SRAS (pathogénicité).
MESH :
- génétique : Glycogen Synthase Kinase 3, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- métabolisme : Glycogen Synthase Kinase 3, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- pathogénicité : Virus du SRAS.
Pascal (Inist)
- Animaux, Apoptose, Cellules Vero, Humains, Multiplication cellulaire, Apoptose, Mort cellulaire, Microbiologie, Immunologie, Phosphorylation, Prolifération cellulaire, Régulation de l'expression des gènes, Syndrome respiratoire aigu sévère, Transduction du signal.
Wicri :
- topic : Immunologie.

English descriptors

KwdEn :
- Animals, Apoptosis, Cell Proliferation, Cell death, Cell proliferation, Chlorocebus aethiops, Gene Expression Regulation, Glycogen Synthase Kinase 3 (genetics), Glycogen Synthase Kinase 3 (metabolism), Humans, Immunology, Microbiology, Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Phosphorylation, Proto-Oncogene Proteins c-akt (genetics), Proto-Oncogene Proteins c-akt (metabolism), SARS Virus (pathogenicity), Severe acute respiratory syndrome, Signal Transduction, Vero Cells.
MESH :
- chemical , genetics : Glycogen Synthase Kinase 3, Proto-Oncogene Proteins c-akt.
- chemical , metabolism : Glycogen Synthase Kinase 3, Proto-Oncogene Proteins c-akt.
- genetics : Phosphatidylinositol 3-Kinases.
- metabolism : Phosphatidylinositol 3-Kinases.
- pathogenicity : SARS Virus.
- Animals, Apoptosis, Cell Proliferation, Chlorocebus aethiops, Gene Expression Regulation, Humans, Phosphorylation, Signal Transduction, Vero Cells.

Abstract

Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (SARS-CoV). Infection of Vero E6 cells with SARS-CoV inhibits cell proliferation. Our previous study indicated that Akt, which is poorly phosphorylated in confluent cultures of Vero E6 cells, is phosphorylated and then dephosphorylated upon infection by SARS-CoV. In the present study, we showed that a serine residue of Akt was phosphorylated in Vero E6 cells in subconfluent culture and that Akt was dephosphorylated rapidly after SARS-CoV infection without up-regulation of its phosphorylation. Phosphorylation of glycogen synthase kinase-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β signaling pathway was not related to inhibition of cell proliferation. Treatment of Vero E6 cells with the phosphatidylinositol 3'-kinase/Akt inhibitor, LY294002, which induces dephosphorylation of Akt, inhibited cell proliferation. As shown in our previous studies, apoptosis occurred in virus-infected cells within 18 h postinfection. Cellular mRNA transcription, which was reported to be up-regulated in SARS-CoV-infected Caco-2 cells, was not up-regulated in virus-infected Vero E6 cells, partially as a result of apoptosis. These results suggested that inhibition of cell proliferation is regulated by both the phosphatidylinositol 3'-kinase/Akt signaling pathway and by apoptosis in SARS-CoV-infected Vero E6 cells. This is the first study to analyze SARS-CoV-induced cell growth inhibition.

Affiliations:

Le document en format XML

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<term>Apoptosis</term>
<term>Cell Proliferation</term>
<term>Cell death</term>
<term>Cell proliferation</term>
<term>Chlorocebus aethiops</term>
<term>Gene Expression Regulation</term>
<term>Glycogen Synthase Kinase 3 (genetics)</term>
<term>Glycogen Synthase Kinase 3 (metabolism)</term>
<term>Humans</term>
<term>Immunology</term>
<term>Microbiology</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Phosphorylation</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>SARS Virus (pathogenicity)</term>
<term>Severe acute respiratory syndrome</term>
<term>Signal Transduction</term>
<term>Vero Cells</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cellules Vero</term>
<term>Glycogen Synthase Kinase 3 (génétique)</term>
<term>Glycogen Synthase Kinase 3 (métabolisme)</term>
<term>Humains</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Régulation de l'expression des gènes</term>
<term>Transduction du signal</term>
<term>Virus du SRAS (pathogénicité)</term>
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<term>Proto-Oncogene Proteins c-akt</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glycogen Synthase Kinase 3</term>
<term>Proto-Oncogene Proteins c-akt</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term>
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<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term>
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<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</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>Apoptosis</term>
<term>Cell Proliferation</term>
<term>Chlorocebus aethiops</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Phosphorylation</term>
<term>Signal Transduction</term>
<term>Vero Cells</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cellules Vero</term>
<term>Humains</term>
<term>Multiplication cellulaire</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
<term>Microbiologie</term>
<term>Immunologie</term>
<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Immunologie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (SARS-CoV). Infection of Vero E6 cells with SARS-CoV inhibits cell proliferation. Our previous study indicated that Akt, which is poorly phosphorylated in confluent cultures of Vero E6 cells, is phosphorylated and then dephosphorylated upon infection by SARS-CoV. In the present study, we showed that a serine residue of Akt was phosphorylated in Vero E6 cells in subconfluent culture and that Akt was dephosphorylated rapidly after SARS-CoV infection without up-regulation of its phosphorylation. Phosphorylation of glycogen synthase kinase-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β signaling pathway was not related to inhibition of cell proliferation. Treatment of Vero E6 cells with the phosphatidylinositol 3'-kinase/Akt inhibitor, LY294002, which induces dephosphorylation of Akt, inhibited cell proliferation. As shown in our previous studies, apoptosis occurred in virus-infected cells within 18 h postinfection. Cellular mRNA transcription, which was reported to be up-regulated in SARS-CoV-infected Caco-2 cells, was not up-regulated in virus-infected Vero E6 cells, partially as a result of apoptosis. These results suggested that inhibition of cell proliferation is regulated by both the phosphatidylinositol 3'-kinase/Akt signaling pathway and by apoptosis in SARS-CoV-infected Vero E6 cells. This is the first study to analyze SARS-CoV-induced cell growth inhibition.</div>
</front>
</TEI>
<affiliations><list><country><li>Japon</li>
</country>
<region><li>Région de Kantō</li>
</region>
<settlement><li>Tokyo</li>
</settlement>
</list>
<tree><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>
<name sortKey="Fukushi, Shuetsu" sort="Fukushi, Shuetsu" uniqKey="Fukushi S" first="Shuetsu" last="Fukushi">Shuetsu Fukushi</name>
<name sortKey="Inanami, Osamu" sort="Inanami, Osamu" uniqKey="Inanami O" first="Osamu" last="Inanami">Osamu Inanami</name>
<name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name>
<name sortKey="Kuwabara, Mikinori" sort="Kuwabara, Mikinori" uniqKey="Kuwabara M" first="Mikinori" last="Kuwabara">Mikinori Kuwabara</name>
<name sortKey="Lizuka, Daisuke" sort="Lizuka, Daisuke" uniqKey="Lizuka D" first="Daisuke" last="Lizuka">Daisuke Lizuka</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>
<name sortKey="Takashima, Hideaki" sort="Takashima, Hideaki" uniqKey="Takashima H" first="Hideaki" last="Takashima">Hideaki Takashima</name>
<name sortKey="Yanagawa, Hiroshi" sort="Yanagawa, Hiroshi" uniqKey="Yanagawa H" first="Hiroshi" last="Yanagawa">Hiroshi Yanagawa</name>
</country>
</tree>
</affiliations>
</record>

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Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells

Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells

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