The involvement of survival signaling pathways in rubella-virus induced apoptosis
Identifieur interne : 000F89 ( Main/Exploration ); précédent : 000F88; suivant : 000F90The involvement of survival signaling pathways in rubella-virus induced apoptosis
Auteurs : Samantha Cooray [Royaume-Uni] ; Li Jin [Royaume-Uni] ; Jennifer M. Best [Royaume-Uni]Source :
- Virology Journal [ 1743-422X ] ; 2005.
Abstract
Rubella virus (RV) causes severe congenital defects when acquired during the first trimester of pregnancy. RV cytopathic effect has been shown to be due to caspase-dependent apoptosis in a number of susceptible cell lines, and it has been suggested that this apoptotic induction could be a causal factor in the development of such defects. Often the outcome of apoptotic stimuli is dependent on apoptotic, proliferative and survival signaling mechanisms in the cell. Therefore we investigated the role of phosphoinositide 3-kinase (PI3K)-Akt survival signaling and Ras-Raf-MEK-ERK proliferative signaling during RV-induced apoptosis in RK13 cells. Increasing levels of phosphorylated ERK, Akt and GSK3β were detected from 24–96 hours post-infection, concomitant with RV-induced apoptotic signals. Inhibition of PI3K-Akt signaling reduced cell viability, and increased the speed and magnitude of RV-induced apoptosis, suggesting that this pathway contributes to cell survival during RV infection. In contrast, inhibition of the Ras-Raf-MEK-ERK pathway impaired RV replication and growth and reduced RV-induced apoptosis, suggesting that the normal cellular growth is required for efficient virus production.
Url:
DOI: 10.1186/1743-422X-2-1
PubMed: 15631631
PubMed Central: 544859
Affiliations:
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Le document en format XML
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Best</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Infectious Diseases, Virology Section, Guy's, King's and St. Thomas' School of Medicine, St. Thomas' Hospital, London SE1 7EH, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Infectious Diseases, Virology Section, Guy's, King's and St. Thomas' School of Medicine, St. Thomas' Hospital, London SE1 7EH</wicri:regionArea><wicri:noRegion>London SE1 7EH</wicri:noRegion></affiliation></author></analytic><series><title level="j">Virology Journal</title><idno type="eISSN">1743-422X</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Rubella virus (RV) causes severe congenital defects when acquired during the first trimester of pregnancy. RV cytopathic effect has been shown to be due to caspase-dependent apoptosis in a number of susceptible cell lines, and it has been suggested that this apoptotic induction could be a causal factor in the development of such defects. Often the outcome of apoptotic stimuli is dependent on apoptotic, proliferative and survival signaling mechanisms in the cell. Therefore we investigated the role of phosphoinositide 3-kinase (PI3K)-Akt survival signaling and Ras-Raf-MEK-ERK proliferative signaling during RV-induced apoptosis in RK13 cells. Increasing levels of phosphorylated ERK, Akt and GSK3β were detected from 24–96 hours post-infection, concomitant with RV-induced apoptotic signals. Inhibition of PI3K-Akt signaling reduced cell viability, and increased the speed and magnitude of RV-induced apoptosis, suggesting that this pathway contributes to cell survival during RV infection. In contrast, inhibition of the Ras-Raf-MEK-ERK pathway impaired RV replication and growth and reduced RV-induced apoptosis, suggesting that the normal cellular growth is required for efficient virus production.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Royaume-Uni</li></country></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Cooray, Samantha" sort="Cooray, Samantha" uniqKey="Cooray S" first="Samantha" last="Cooray">Samantha Cooray</name></noRegion><name sortKey="Best, Jennifer M" sort="Best, Jennifer M" uniqKey="Best J" first="Jennifer M" last="Best">Jennifer M. Best</name><name sortKey="Cooray, Samantha" sort="Cooray, Samantha" uniqKey="Cooray S" first="Samantha" last="Cooray">Samantha Cooray</name><name sortKey="Cooray, Samantha" sort="Cooray, Samantha" uniqKey="Cooray S" first="Samantha" last="Cooray">Samantha Cooray</name><name sortKey="Jin, Li" sort="Jin, Li" uniqKey="Jin L" first="Li" last="Jin">Li Jin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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