mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells.
Identifieur interne : 000F40 ( Main/Exploration ); précédent : 000F39; suivant : 000F41mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells.
Auteurs : Gordana Tovilovic [Serbie] ; Biljana Ristic ; Marina Siljic ; Valentina Nikolic ; Tamara Kravic-Stevovic ; Marija Dulovic ; Marina Milenkovic ; Aleksandra Knezevic ; Mihajlo Bosnjak ; Vladimir Bumbasirevic ; Maja Stanojevic ; Vladimir TrajkovicSource :
- Microbes and infection [ 1769-714X ]
Descripteurs français
- KwdFr :
- Apoptose (MeSH), Autophagie (MeSH), Herpèsvirus humain de type 1 (immunologie), Herpèsvirus humain de type 1 (pathogénicité), Humains (MeSH), Interactions hôte-pathogène (MeSH), Lignée cellulaire (MeSH), Névroglie (immunologie), Névroglie (virologie), Régulation de l'expression des gènes (MeSH), Survie cellulaire (MeSH), Sérine-thréonine kinases TOR (métabolisme).
- MESH :
- immunologie : Herpèsvirus humain de type 1, Névroglie.
- métabolisme : Sérine-thréonine kinases TOR.
- pathogénicité : Herpèsvirus humain de type 1.
- virologie : Névroglie.
- Apoptose, Autophagie, Humains, Interactions hôte-pathogène, Lignée cellulaire, Régulation de l'expression des gènes, Survie cellulaire.
English descriptors
- KwdEn :
- Apoptosis (MeSH), Autophagy (MeSH), Cell Line (MeSH), Cell Survival (MeSH), Gene Expression Regulation (MeSH), Herpesvirus 1, Human (immunology), Herpesvirus 1, Human (pathogenicity), Host-Pathogen Interactions (MeSH), Humans (MeSH), Neuroglia (immunology), Neuroglia (virology), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , metabolism : TOR Serine-Threonine Kinases.
- immunology : Herpesvirus 1, Human, Neuroglia.
- pathogenicity : Herpesvirus 1, Human.
- virology : Neuroglia.
- Apoptosis, Autophagy, Cell Line, Cell Survival, Gene Expression Regulation, Host-Pathogen Interactions, Humans.
Abstract
We investigated the role of autophagy, a stress-inducible lysosomal self-digestion of cellular components, in modulation of herpes simplex virus type 1 (HSV-1)-triggered death of U251 human glioma cells. HSV-1 caused apoptotic death in U251 cells, characterized by phosphatidylserine externalization, caspase activation and DNA fragmentation. HSV-1-induced apoptosis was associated with the induction of autophagic response, as confirmed by the conversion of cytosolic LC3-I to autophagosome-associated LC3-II, increase in intracellular acidification, presence of autophagic vesicles, and increase in proteolysis of the selective autophagic target p62. HSV-1-triggered autophagy was not associated with the significant increase in the expression of proautophagic protein beclin-1 or downregulation of the major autophagy suppressor mammalian target of rapamycin (mTOR). Moreover, the phosphorylation of mTOR and its direct substrate p70 S6 kinase was augmented by HSV-1 infection, while the mTOR stimulator Akt and inhibitor AMPK-activated protein kinase (AMPK) were accordingly activated and suppressed, respectively. An shRNA-mediated knockdown of the autophagy-essential LC3β, as well as pharmacological inhibition of autophagy with bafilomycin A1 or 3-methyladenine, markedly accelerated apoptotic changes and ensuing cell death in HSV-1-infected glioma cells. These data indicate that AMPK/Akt/mTOR-independent autophagy could prolong survival of HSV-1-infected U251 glioma cells by counteracting the coinciding apoptotic response.
DOI: 10.1016/j.micinf.2013.04.012
PubMed: 23669212
Affiliations:
Links toward previous steps (curation, corpus...)
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sortKey="Siljic, Marina" sort="Siljic, Marina" uniqKey="Siljic M" first="Marina" last="Siljic">Marina Siljic</name></author><author><name sortKey="Nikolic, Valentina" sort="Nikolic, Valentina" uniqKey="Nikolic V" first="Valentina" last="Nikolic">Valentina Nikolic</name></author><author><name sortKey="Kravic Stevovic, Tamara" sort="Kravic Stevovic, Tamara" uniqKey="Kravic Stevovic T" first="Tamara" last="Kravic-Stevovic">Tamara Kravic-Stevovic</name></author><author><name sortKey="Dulovic, Marija" sort="Dulovic, Marija" uniqKey="Dulovic M" first="Marija" last="Dulovic">Marija Dulovic</name></author><author><name sortKey="Milenkovic, Marina" sort="Milenkovic, Marina" uniqKey="Milenkovic M" first="Marina" last="Milenkovic">Marina Milenkovic</name></author><author><name sortKey="Knezevic, Aleksandra" sort="Knezevic, Aleksandra" uniqKey="Knezevic A" first="Aleksandra" last="Knezevic">Aleksandra Knezevic</name></author><author><name sortKey="Bosnjak, Mihajlo" sort="Bosnjak, Mihajlo" uniqKey="Bosnjak M" first="Mihajlo" last="Bosnjak">Mihajlo Bosnjak</name></author><author><name sortKey="Bumbasirevic, Vladimir" sort="Bumbasirevic, Vladimir" uniqKey="Bumbasirevic V" first="Vladimir" last="Bumbasirevic">Vladimir Bumbasirevic</name></author><author><name sortKey="Stanojevic, Maja" sort="Stanojevic, Maja" uniqKey="Stanojevic M" first="Maja" last="Stanojevic">Maja Stanojevic</name></author><author><name sortKey="Trajkovic, Vladimir" sort="Trajkovic, Vladimir" uniqKey="Trajkovic V" first="Vladimir" last="Trajkovic">Vladimir Trajkovic</name></author></analytic><series><title level="j">Microbes and infection</title><idno type="eISSN">1769-714X</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (MeSH)</term><term>Autophagy (MeSH)</term><term>Cell Line (MeSH)</term><term>Cell Survival (MeSH)</term><term>Gene Expression Regulation (MeSH)</term><term>Herpesvirus 1, Human (immunology)</term><term>Herpesvirus 1, Human (pathogenicity)</term><term>Host-Pathogen Interactions (MeSH)</term><term>Humans (MeSH)</term><term>Neuroglia (immunology)</term><term>Neuroglia (virology)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose (MeSH)</term><term>Autophagie (MeSH)</term><term>Herpèsvirus humain de type 1 (immunologie)</term><term>Herpèsvirus humain de type 1 (pathogénicité)</term><term>Humains (MeSH)</term><term>Interactions hôte-pathogène (MeSH)</term><term>Lignée cellulaire (MeSH)</term><term>Névroglie (immunologie)</term><term>Névroglie (virologie)</term><term>Régulation de l'expression des gènes (MeSH)</term><term>Survie cellulaire (MeSH)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Herpèsvirus humain de type 1</term><term>Névroglie</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Herpesvirus 1, Human</term><term>Neuroglia</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Herpesvirus 1, Human</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Herpèsvirus humain de type 1</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Névroglie</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Neuroglia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Line</term><term>Cell Survival</term><term>Gene Expression Regulation</term><term>Host-Pathogen Interactions</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Lignée cellulaire</term><term>Régulation de l'expression des gènes</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated the role of autophagy, a stress-inducible lysosomal self-digestion of cellular components, in modulation of herpes simplex virus type 1 (HSV-1)-triggered death of U251 human glioma cells. HSV-1 caused apoptotic death in U251 cells, characterized by phosphatidylserine externalization, caspase activation and DNA fragmentation. HSV-1-induced apoptosis was associated with the induction of autophagic response, as confirmed by the conversion of cytosolic LC3-I to autophagosome-associated LC3-II, increase in intracellular acidification, presence of autophagic vesicles, and increase in proteolysis of the selective autophagic target p62. HSV-1-triggered autophagy was not associated with the significant increase in the expression of proautophagic protein beclin-1 or downregulation of the major autophagy suppressor mammalian target of rapamycin (mTOR). Moreover, the phosphorylation of mTOR and its direct substrate p70 S6 kinase was augmented by HSV-1 infection, while the mTOR stimulator Akt and inhibitor AMPK-activated protein kinase (AMPK) were accordingly activated and suppressed, respectively. An shRNA-mediated knockdown of the autophagy-essential LC3β, as well as pharmacological inhibition of autophagy with bafilomycin A1 or 3-methyladenine, markedly accelerated apoptotic changes and ensuing cell death in HSV-1-infected glioma cells. These data indicate that AMPK/Akt/mTOR-independent autophagy could prolong survival of HSV-1-infected U251 glioma cells by counteracting the coinciding apoptotic response. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23669212</PMID><DateCompleted><Year>2014</Year><Month>02</Month><Day>07</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1769-714X</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>8-9</Issue><PubDate><MedlineDate>2013 Jul-Aug</MedlineDate></PubDate></JournalIssue><Title>Microbes and infection</Title><ISOAbbreviation>Microbes Infect</ISOAbbreviation></Journal><ArticleTitle>mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells.</ArticleTitle><Pagination><MedlinePgn>615-24</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.micinf.2013.04.012</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1286-4579(13)00093-2</ELocationID><Abstract><AbstractText>We investigated the role of autophagy, a stress-inducible lysosomal self-digestion of cellular components, in modulation of herpes simplex virus type 1 (HSV-1)-triggered death of U251 human glioma cells. HSV-1 caused apoptotic death in U251 cells, characterized by phosphatidylserine externalization, caspase activation and DNA fragmentation. HSV-1-induced apoptosis was associated with the induction of autophagic response, as confirmed by the conversion of cytosolic LC3-I to autophagosome-associated LC3-II, increase in intracellular acidification, presence of autophagic vesicles, and increase in proteolysis of the selective autophagic target p62. HSV-1-triggered autophagy was not associated with the significant increase in the expression of proautophagic protein beclin-1 or downregulation of the major autophagy suppressor mammalian target of rapamycin (mTOR). Moreover, the phosphorylation of mTOR and its direct substrate p70 S6 kinase was augmented by HSV-1 infection, while the mTOR stimulator Akt and inhibitor AMPK-activated protein kinase (AMPK) were accordingly activated and suppressed, respectively. An shRNA-mediated knockdown of the autophagy-essential LC3β, as well as pharmacological inhibition of autophagy with bafilomycin A1 or 3-methyladenine, markedly accelerated apoptotic changes and ensuing cell death in HSV-1-infected glioma cells. These data indicate that AMPK/Akt/mTOR-independent autophagy could prolong survival of HSV-1-infected U251 glioma cells by counteracting the coinciding apoptotic response. </AbstractText><CopyrightInformation>Copyright © 2013 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tovilovic</LastName><ForeName>Gordana</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Institute for Biological Research, University of Belgrade, Despota Stefana Blvd.142, 11000 Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ristic</LastName><ForeName>Biljana</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Siljic</LastName><ForeName>Marina</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Nikolic</LastName><ForeName>Valentina</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Kravic-Stevovic</LastName><ForeName>Tamara</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Dulovic</LastName><ForeName>Marija</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Milenkovic</LastName><ForeName>Marina</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Knezevic</LastName><ForeName>Aleksandra</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Bosnjak</LastName><ForeName>Mihajlo</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Bumbasirevic</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Stanojevic</LastName><ForeName>Maja</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Trajkovic</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>05</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Microbes Infect</MedlineTA><NlmUniqueID>100883508</NlmUniqueID><ISSNLinking>1286-4579</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018259" MajorTopicYN="N">Herpesvirus 1, Human</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009457" MajorTopicYN="N">Neuroglia</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">AMP-activated protein kinase</Keyword><Keyword MajorTopicYN="N">Akt</Keyword><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">HSV-1</Keyword><Keyword MajorTopicYN="N">mTOR</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>08</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>01</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>04</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>5</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>5</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>2</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23669212</ArticleId><ArticleId IdType="pii">S1286-4579(13)00093-2</ArticleId><ArticleId IdType="doi">10.1016/j.micinf.2013.04.012</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Serbie</li></country></list><tree><noCountry><name sortKey="Bosnjak, Mihajlo" sort="Bosnjak, Mihajlo" uniqKey="Bosnjak M" first="Mihajlo" last="Bosnjak">Mihajlo Bosnjak</name><name sortKey="Bumbasirevic, Vladimir" sort="Bumbasirevic, Vladimir" uniqKey="Bumbasirevic V" first="Vladimir" last="Bumbasirevic">Vladimir Bumbasirevic</name><name sortKey="Dulovic, Marija" sort="Dulovic, Marija" uniqKey="Dulovic M" first="Marija" last="Dulovic">Marija Dulovic</name><name sortKey="Knezevic, Aleksandra" sort="Knezevic, Aleksandra" uniqKey="Knezevic A" first="Aleksandra" last="Knezevic">Aleksandra Knezevic</name><name sortKey="Kravic Stevovic, Tamara" sort="Kravic Stevovic, Tamara" uniqKey="Kravic Stevovic T" first="Tamara" last="Kravic-Stevovic">Tamara Kravic-Stevovic</name><name sortKey="Milenkovic, Marina" sort="Milenkovic, Marina" uniqKey="Milenkovic M" first="Marina" last="Milenkovic">Marina Milenkovic</name><name sortKey="Nikolic, Valentina" sort="Nikolic, Valentina" uniqKey="Nikolic V" first="Valentina" last="Nikolic">Valentina Nikolic</name><name sortKey="Ristic, Biljana" sort="Ristic, Biljana" uniqKey="Ristic B" first="Biljana" last="Ristic">Biljana Ristic</name><name sortKey="Siljic, Marina" sort="Siljic, Marina" uniqKey="Siljic M" first="Marina" last="Siljic">Marina Siljic</name><name sortKey="Stanojevic, Maja" sort="Stanojevic, Maja" uniqKey="Stanojevic M" first="Maja" last="Stanojevic">Maja Stanojevic</name><name sortKey="Trajkovic, Vladimir" sort="Trajkovic, Vladimir" uniqKey="Trajkovic V" first="Vladimir" last="Trajkovic">Vladimir Trajkovic</name></noCountry><country name="Serbie"><noRegion><name sortKey="Tovilovic, Gordana" sort="Tovilovic, Gordana" uniqKey="Tovilovic G" first="Gordana" last="Tovilovic">Gordana Tovilovic</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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