Osteopontin counters human immunodeficiency virus type 1-induced impairment of neurite growth through mammalian target of rapamycin and beta-integrin signaling pathways.
Identifieur interne : 000265 ( Main/Exploration ); précédent : 000264; suivant : 000266Osteopontin counters human immunodeficiency virus type 1-induced impairment of neurite growth through mammalian target of rapamycin and beta-integrin signaling pathways.
Auteurs : Mathilde Calvez [France] ; George Hseeh [États-Unis] ; Simon Benzer [États-Unis] ; Amanda M. Brown [États-Unis]Source :
- Journal of neurovirology [ 1538-2443 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Chaines bêta des intégrines (métabolisme), Démence associée au SIDA (métabolisme), Humains (MeSH), Neurites (métabolisme), Neurites (virologie), Ostéopontine (métabolisme), Produits du gène env du virus de l'immunodéficience humaine (MeSH), Rats (MeSH), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (physiologie), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (MeSH).
- MESH :
- métabolisme : Chaines bêta des intégrines, Démence associée au SIDA, Neurites, Ostéopontine, Sérine-thréonine kinases TOR.
- physiologie : Transduction du signal.
- virologie : Neurites.
- Animaux, Cellules cultivées, Humains, Produits du gène env du virus de l'immunodéficience humaine, Rats, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
English descriptors
- KwdEn :
- AIDS Dementia Complex (metabolism), Animals (MeSH), Cells, Cultured (MeSH), HIV-1 (MeSH), Humans (MeSH), Integrin beta Chains (metabolism), Neurites (metabolism), Neurites (virology), Osteopontin (metabolism), Rats (MeSH), Signal Transduction (physiology), TOR Serine-Threonine Kinases (metabolism), env Gene Products, Human Immunodeficiency Virus (MeSH).
- MESH :
- chemical , metabolism : Integrin beta Chains, Osteopontin, TOR Serine-Threonine Kinases.
- metabolism : AIDS Dementia Complex, Neurites.
- physiology : Signal Transduction.
- virology : Neurites.
- Animals, Cells, Cultured, HIV-1, Humans, Rats, env Gene Products, Human Immunodeficiency Virus.
Abstract
Despite the fact that human immunodeficiency virus type 1 (HIV-1) does not enter or replicate in neurons, its infection of a subset of resident brain glia cells (microglia and astrocytes) induces via disparate mechanisms, dysregulation of glutamate metabolism, neurotoxicity, and inflammation. Antiretroviral therapies suppress viral load, but cellular activation and release of proinflammatory factors, some of which is likely related to viral reservoirs, continue to promote a microenvironment that is injurious to neurons. However, the molecular mechanisms remain to be identified. Osteopontin (OPN) is a proinflammatory cytokine-like, extracellular matrix protein that is elevated within the brain and CSF in several neurodegenerative disorders, including HIV-associated cognitive disorder. However, the impact of elevated OPN on neuronal integrity and function in HIV-infected individuals who exhibit cognitive dysfunction remains unknown. In this study, using a neuronal cell line and primary cultures of cortical rat neurons, we identify the mammalian target of rapamycin pathway involvement in a signaling interaction between OPN-β1-integrins and the HIV-1 envelope glycoprotein, which stimulates neurite growth. These findings link for the first time HIV X4-envelope receptor engagement and osteopontin-mediated signaling through β1-integrin receptors to the mTOR pathway and alterations in the cytoskeleton of cortical neurons.
DOI: 10.1007/s13365-019-00729-y
PubMed: 30758811
PubMed Central: PMC6647884
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Brown</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 6-119, Baltimore, MD, 21287, USA. abrown76@jhmi.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 6-119, Baltimore, MD, 21287</wicri:regionArea><wicri:noRegion>21287</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of neurovirology</title><idno type="eISSN">1538-2443</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AIDS Dementia Complex (metabolism)</term><term>Animals (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>HIV-1 (MeSH)</term><term>Humans (MeSH)</term><term>Integrin beta Chains (metabolism)</term><term>Neurites (metabolism)</term><term>Neurites (virology)</term><term>Osteopontin (metabolism)</term><term>Rats (MeSH)</term><term>Signal Transduction (physiology)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>env Gene Products, Human Immunodeficiency Virus (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Chaines bêta des intégrines (métabolisme)</term><term>Démence associée au SIDA (métabolisme)</term><term>Humains (MeSH)</term><term>Neurites (métabolisme)</term><term>Neurites (virologie)</term><term>Ostéopontine (métabolisme)</term><term>Produits du gène env du virus de l'immunodéficience humaine (MeSH)</term><term>Rats (MeSH)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (physiologie)</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Integrin beta Chains</term><term>Osteopontin</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>AIDS Dementia Complex</term><term>Neurites</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Chaines bêta des intégrines</term><term>Démence associée au SIDA</term><term>Neurites</term><term>Ostéopontine</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Neurites</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Neurites</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>HIV-1</term><term>Humans</term><term>Rats</term><term>env Gene Products, Human Immunodeficiency Virus</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Humains</term><term>Produits du gène env du virus de l'immunodéficience humaine</term><term>Rats</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite the fact that human immunodeficiency virus type 1 (HIV-1) does not enter or replicate in neurons, its infection of a subset of resident brain glia cells (microglia and astrocytes) induces via disparate mechanisms, dysregulation of glutamate metabolism, neurotoxicity, and inflammation. Antiretroviral therapies suppress viral load, but cellular activation and release of proinflammatory factors, some of which is likely related to viral reservoirs, continue to promote a microenvironment that is injurious to neurons. However, the molecular mechanisms remain to be identified. Osteopontin (OPN) is a proinflammatory cytokine-like, extracellular matrix protein that is elevated within the brain and CSF in several neurodegenerative disorders, including HIV-associated cognitive disorder. However, the impact of elevated OPN on neuronal integrity and function in HIV-infected individuals who exhibit cognitive dysfunction remains unknown. In this study, using a neuronal cell line and primary cultures of cortical rat neurons, we identify the mammalian target of rapamycin pathway involvement in a signaling interaction between OPN-β1-integrins and the HIV-1 envelope glycoprotein, which stimulates neurite growth. These findings link for the first time HIV X4-envelope receptor engagement and osteopontin-mediated signaling through β1-integrin receptors to the mTOR pathway and alterations in the cytoskeleton of cortical neurons.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30758811</PMID><DateCompleted><Year>2020</Year><Month>09</Month><Day>22</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1538-2443</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>3</Issue><PubDate><Year>2019</Year><Month>06</Month></PubDate></JournalIssue><Title>Journal of neurovirology</Title><ISOAbbreviation>J Neurovirol</ISOAbbreviation></Journal><ArticleTitle>Osteopontin counters human immunodeficiency virus type 1-induced impairment of neurite growth through mammalian target of rapamycin and beta-integrin signaling pathways.</ArticleTitle><Pagination><MedlinePgn>384-396</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s13365-019-00729-y</ELocationID><Abstract><AbstractText>Despite the fact that human immunodeficiency virus type 1 (HIV-1) does not enter or replicate in neurons, its infection of a subset of resident brain glia cells (microglia and astrocytes) induces via disparate mechanisms, dysregulation of glutamate metabolism, neurotoxicity, and inflammation. Antiretroviral therapies suppress viral load, but cellular activation and release of proinflammatory factors, some of which is likely related to viral reservoirs, continue to promote a microenvironment that is injurious to neurons. However, the molecular mechanisms remain to be identified. Osteopontin (OPN) is a proinflammatory cytokine-like, extracellular matrix protein that is elevated within the brain and CSF in several neurodegenerative disorders, including HIV-associated cognitive disorder. However, the impact of elevated OPN on neuronal integrity and function in HIV-infected individuals who exhibit cognitive dysfunction remains unknown. In this study, using a neuronal cell line and primary cultures of cortical rat neurons, we identify the mammalian target of rapamycin pathway involvement in a signaling interaction between OPN-β1-integrins and the HIV-1 envelope glycoprotein, which stimulates neurite growth. These findings link for the first time HIV X4-envelope receptor engagement and osteopontin-mediated signaling through β1-integrin receptors to the mTOR pathway and alterations in the cytoskeleton of cortical neurons.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Calvez</LastName><ForeName>Mathilde</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Biology, Ecole Normale Superieure de Lyon, Lyon, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hseeh</LastName><ForeName>George</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 6-119, Baltimore, MD, 21287, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benzer</LastName><ForeName>Simon</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 6-119, Baltimore, MD, 21287, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brown</LastName><ForeName>Amanda M</ForeName><Initials>AM</Initials><Identifier Source="ORCID">0000-0002-4576-9636</Identifier><AffiliationInfo><Affiliation>Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 6-119, Baltimore, MD, 21287, USA. abrown76@jhmi.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS102006</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 MH095646</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R25 MH080661</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>02</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurovirol</MedlineTA><NlmUniqueID>9508123</NlmUniqueID><ISSNLinking>1355-0284</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039641">Integrin beta Chains</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054299">env Gene Products, Human Immunodeficiency Virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>106441-73-0</RegistryNumber><NameOfSubstance UI="D053495">Osteopontin</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="D015526" MajorTopicYN="N">AIDS Dementia Complex</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015497" MajorTopicYN="N">HIV-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D039641" MajorTopicYN="N">Integrin beta Chains</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016501" MajorTopicYN="N">Neurites</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053495" MajorTopicYN="N">Osteopontin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054299" MajorTopicYN="N">env Gene Products, Human Immunodeficiency Virus</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cytoskeleton</Keyword><Keyword MajorTopicYN="Y">Dendrites</Keyword><Keyword MajorTopicYN="Y">HIV-associated neurocognitive disorder</Keyword><Keyword MajorTopicYN="Y">Integrins</Keyword><Keyword MajorTopicYN="Y">Neurons</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>01</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>01</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>2</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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