Mitochondria Influence Fas Expression in GP120-Induced Apoptosis of Neuronal Cells
The human immunodeficiency virus-1 (HIV-1) destroys the immune system and also induces neurological disease culminating into dementia (HIV-associated dementia). Though the HIV viral protein gp120 induces apoptosis in neuronal cells, the mechanism of action is still poorly defined. Recent studies sho...
Gespeichert in:
| Veröffentlicht in: | International journal of neuroscience 2009-01, Vol.119 (2), p.157-165 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 165 |
|---|---|
| container_issue | 2 |
| container_start_page | 157 |
| container_title | International journal of neuroscience |
| container_volume | 119 |
| creator | Thomas, Sunil Mayer, Lloyd Sperber, Kirk |
| description | The human immunodeficiency virus-1 (HIV-1) destroys the immune system and also induces neurological disease culminating into dementia (HIV-associated dementia). Though the HIV viral protein gp120 induces apoptosis in neuronal cells, the mechanism of action is still poorly defined. Recent studies show that cells die during apoptosis by Fas aggregation aided by the mitochondrial proapoptotic proteins. Our studies show an increase in expression of Fas and its associated downstream proteins after treatment of the neuroblastoma cells, SH-SY5Y, with gp120. Fas and its associated death proteins, FADD and caspase-8 (DISC), are downregulated when treated with the caspase inhibitors. The results indicate that mitochondrial-death proteins like caspases may influence the upregulation of the death receptor Fas, and the inhibition of caspases prevents gp120-induced apoptosis. |
| doi_str_mv | 10.1080/00207450802335537 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_infor</sourceid><recordid>TN_cdi_proquest_miscellaneous_66796146</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>66796146</sourcerecordid><originalsourceid>FETCH-LOGICAL-c404t-7d486f606fcc090af8734a4240b4c381931c7e05b45010a98aef9174bec9d5903</originalsourceid><addsrcrecordid>eNp9kEtLAzEYRYMottT-ADeSlbvRZJJ5BN2U0tZCfSC6DplMQiPTZExm0P57U1oQEbpKQs65fN8F4BKjG4xKdItQigqaxWtKSJaR4gQMcZaTJEsLdgqGu_8kAnQAxiGYKr4JY2lZnoMBZjiNBh6C10fTObl2tvZGwKXVTa-sVHAuApx9t15F1VloLFy84Bi4tHUvVQ0nrWs7F0yATsMn1XtnRQOnqmnCBTjToglqfDhH4H0-e5s-JKvnxXI6WSWSItolRU3LXOco11IihoQuC0IFTSmqqCQlZgTLQqGsijtiJFgplGa4oJWSrM4YIiNwvc9tvfvsVej4xgQZJxBWuT7wPC9YjmkeQbwHpXcheKV5681G-C3HiO-65P-6jM7VIbyvNqr-NQ7NReB-Dxirnd-IL-ebmndi2zivvbDSBE6O5d_90ddKNN1aCq_4h-t9LDMcme4HaNGSKQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>66796146</pqid></control><display><type>article</type><title>Mitochondria Influence Fas Expression in GP120-Induced Apoptosis of Neuronal Cells</title><source>MEDLINE</source><source>Taylor & Francis:Master (3349 titles)</source><source>Taylor & Francis Medical Library - CRKN</source><creator>Thomas, Sunil ; Mayer, Lloyd ; Sperber, Kirk</creator><creatorcontrib>Thomas, Sunil ; Mayer, Lloyd ; Sperber, Kirk</creatorcontrib><description>The human immunodeficiency virus-1 (HIV-1) destroys the immune system and also induces neurological disease culminating into dementia (HIV-associated dementia). Though the HIV viral protein gp120 induces apoptosis in neuronal cells, the mechanism of action is still poorly defined. Recent studies show that cells die during apoptosis by Fas aggregation aided by the mitochondrial proapoptotic proteins. Our studies show an increase in expression of Fas and its associated downstream proteins after treatment of the neuroblastoma cells, SH-SY5Y, with gp120. Fas and its associated death proteins, FADD and caspase-8 (DISC), are downregulated when treated with the caspase inhibitors. The results indicate that mitochondrial-death proteins like caspases may influence the upregulation of the death receptor Fas, and the inhibition of caspases prevents gp120-induced apoptosis.</description><identifier>ISSN: 0020-7454</identifier><identifier>EISSN: 1563-5279</identifier><identifier>EISSN: 1543-5245</identifier><identifier>DOI: 10.1080/00207450802335537</identifier><identifier>PMID: 19125371</identifier><language>eng</language><publisher>England: Informa UK Ltd</publisher><subject>AIDS Dementia Complex - genetics ; AIDS Dementia Complex - metabolism ; AIDS Dementia Complex - physiopathology ; apoptosis ; Apoptosis - physiology ; Brain - metabolism ; Brain - physiopathology ; caspase ; Caspase 8 - genetics ; Caspase 8 - metabolism ; Cell Line, Tumor ; dementia ; Down-Regulation - physiology ; fas ; fas Receptor - genetics ; fas Receptor - metabolism ; Fas-Associated Death Domain Protein - genetics ; Fas-Associated Death Domain Protein - metabolism ; HIV ; HIV Envelope Protein gp120 - genetics ; HIV Envelope Protein gp120 - metabolism ; HIV-1 - genetics ; HIV-1 - metabolism ; Humans ; mitochondria ; Mitochondria - genetics ; Mitochondria - metabolism ; Nerve Degeneration - genetics ; Nerve Degeneration - metabolism ; Nerve Degeneration - physiopathology ; Neurons - metabolism ; Neurons - pathology ; Up-Regulation - physiology</subject><ispartof>International journal of neuroscience, 2009-01, Vol.119 (2), p.157-165</ispartof><rights>2009 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-7d486f606fcc090af8734a4240b4c381931c7e05b45010a98aef9174bec9d5903</citedby><cites>FETCH-LOGICAL-c404t-7d486f606fcc090af8734a4240b4c381931c7e05b45010a98aef9174bec9d5903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/00207450802335537$$EPDF$$P50$$Ginformahealthcare$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/00207450802335537$$EHTML$$P50$$Ginformahealthcare$$H</linktohtml><link.rule.ids>315,782,786,27931,27932,59654,59760,60443,60549,61228,61263,61409,61444</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19125371$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Thomas, Sunil</creatorcontrib><creatorcontrib>Mayer, Lloyd</creatorcontrib><creatorcontrib>Sperber, Kirk</creatorcontrib><title>Mitochondria Influence Fas Expression in GP120-Induced Apoptosis of Neuronal Cells</title><title>International journal of neuroscience</title><addtitle>Int J Neurosci</addtitle><description>The human immunodeficiency virus-1 (HIV-1) destroys the immune system and also induces neurological disease culminating into dementia (HIV-associated dementia). Though the HIV viral protein gp120 induces apoptosis in neuronal cells, the mechanism of action is still poorly defined. Recent studies show that cells die during apoptosis by Fas aggregation aided by the mitochondrial proapoptotic proteins. Our studies show an increase in expression of Fas and its associated downstream proteins after treatment of the neuroblastoma cells, SH-SY5Y, with gp120. Fas and its associated death proteins, FADD and caspase-8 (DISC), are downregulated when treated with the caspase inhibitors. The results indicate that mitochondrial-death proteins like caspases may influence the upregulation of the death receptor Fas, and the inhibition of caspases prevents gp120-induced apoptosis.</description><subject>AIDS Dementia Complex - genetics</subject><subject>AIDS Dementia Complex - metabolism</subject><subject>AIDS Dementia Complex - physiopathology</subject><subject>apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Brain - metabolism</subject><subject>Brain - physiopathology</subject><subject>caspase</subject><subject>Caspase 8 - genetics</subject><subject>Caspase 8 - metabolism</subject><subject>Cell Line, Tumor</subject><subject>dementia</subject><subject>Down-Regulation - physiology</subject><subject>fas</subject><subject>fas Receptor - genetics</subject><subject>fas Receptor - metabolism</subject><subject>Fas-Associated Death Domain Protein - genetics</subject><subject>Fas-Associated Death Domain Protein - metabolism</subject><subject>HIV</subject><subject>HIV Envelope Protein gp120 - genetics</subject><subject>HIV Envelope Protein gp120 - metabolism</subject><subject>HIV-1 - genetics</subject><subject>HIV-1 - metabolism</subject><subject>Humans</subject><subject>mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Nerve Degeneration - genetics</subject><subject>Nerve Degeneration - metabolism</subject><subject>Nerve Degeneration - physiopathology</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Up-Regulation - physiology</subject><issn>0020-7454</issn><issn>1563-5279</issn><issn>1543-5245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLAzEYRYMottT-ADeSlbvRZJJ5BN2U0tZCfSC6DplMQiPTZExm0P57U1oQEbpKQs65fN8F4BKjG4xKdItQigqaxWtKSJaR4gQMcZaTJEsLdgqGu_8kAnQAxiGYKr4JY2lZnoMBZjiNBh6C10fTObl2tvZGwKXVTa-sVHAuApx9t15F1VloLFy84Bi4tHUvVQ0nrWs7F0yATsMn1XtnRQOnqmnCBTjToglqfDhH4H0-e5s-JKvnxXI6WSWSItolRU3LXOco11IihoQuC0IFTSmqqCQlZgTLQqGsijtiJFgplGa4oJWSrM4YIiNwvc9tvfvsVej4xgQZJxBWuT7wPC9YjmkeQbwHpXcheKV5681G-C3HiO-65P-6jM7VIbyvNqr-NQ7NReB-Dxirnd-IL-ebmndi2zivvbDSBE6O5d_90ddKNN1aCq_4h-t9LDMcme4HaNGSKQ</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Thomas, Sunil</creator><creator>Mayer, Lloyd</creator><creator>Sperber, Kirk</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20090101</creationdate><title>Mitochondria Influence Fas Expression in GP120-Induced Apoptosis of Neuronal Cells</title><author>Thomas, Sunil ; Mayer, Lloyd ; Sperber, Kirk</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-7d486f606fcc090af8734a4240b4c381931c7e05b45010a98aef9174bec9d5903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>AIDS Dementia Complex - genetics</topic><topic>AIDS Dementia Complex - metabolism</topic><topic>AIDS Dementia Complex - physiopathology</topic><topic>apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Brain - metabolism</topic><topic>Brain - physiopathology</topic><topic>caspase</topic><topic>Caspase 8 - genetics</topic><topic>Caspase 8 - metabolism</topic><topic>Cell Line, Tumor</topic><topic>dementia</topic><topic>Down-Regulation - physiology</topic><topic>fas</topic><topic>fas Receptor - genetics</topic><topic>fas Receptor - metabolism</topic><topic>Fas-Associated Death Domain Protein - genetics</topic><topic>Fas-Associated Death Domain Protein - metabolism</topic><topic>HIV</topic><topic>HIV Envelope Protein gp120 - genetics</topic><topic>HIV Envelope Protein gp120 - metabolism</topic><topic>HIV-1 - genetics</topic><topic>HIV-1 - metabolism</topic><topic>Humans</topic><topic>mitochondria</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - metabolism</topic><topic>Nerve Degeneration - genetics</topic><topic>Nerve Degeneration - metabolism</topic><topic>Nerve Degeneration - physiopathology</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Up-Regulation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thomas, Sunil</creatorcontrib><creatorcontrib>Mayer, Lloyd</creatorcontrib><creatorcontrib>Sperber, Kirk</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thomas, Sunil</au><au>Mayer, Lloyd</au><au>Sperber, Kirk</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondria Influence Fas Expression in GP120-Induced Apoptosis of Neuronal Cells</atitle><jtitle>International journal of neuroscience</jtitle><addtitle>Int J Neurosci</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>119</volume><issue>2</issue><spage>157</spage><epage>165</epage><pages>157-165</pages><issn>0020-7454</issn><eissn>1563-5279</eissn><eissn>1543-5245</eissn><abstract>The human immunodeficiency virus-1 (HIV-1) destroys the immune system and also induces neurological disease culminating into dementia (HIV-associated dementia). Though the HIV viral protein gp120 induces apoptosis in neuronal cells, the mechanism of action is still poorly defined. Recent studies show that cells die during apoptosis by Fas aggregation aided by the mitochondrial proapoptotic proteins. Our studies show an increase in expression of Fas and its associated downstream proteins after treatment of the neuroblastoma cells, SH-SY5Y, with gp120. Fas and its associated death proteins, FADD and caspase-8 (DISC), are downregulated when treated with the caspase inhibitors. The results indicate that mitochondrial-death proteins like caspases may influence the upregulation of the death receptor Fas, and the inhibition of caspases prevents gp120-induced apoptosis.</abstract><cop>England</cop><pub>Informa UK Ltd</pub><pmid>19125371</pmid><doi>10.1080/00207450802335537</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0020-7454 |
| ispartof | International journal of neuroscience, 2009-01, Vol.119 (2), p.157-165 |
| issn | 0020-7454 1563-5279 1543-5245 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_66796146 |
| source | MEDLINE; Taylor & Francis:Master (3349 titles); Taylor & Francis Medical Library - CRKN |
| subjects | AIDS Dementia Complex - genetics AIDS Dementia Complex - metabolism AIDS Dementia Complex - physiopathology apoptosis Apoptosis - physiology Brain - metabolism Brain - physiopathology caspase Caspase 8 - genetics Caspase 8 - metabolism Cell Line, Tumor dementia Down-Regulation - physiology fas fas Receptor - genetics fas Receptor - metabolism Fas-Associated Death Domain Protein - genetics Fas-Associated Death Domain Protein - metabolism HIV HIV Envelope Protein gp120 - genetics HIV Envelope Protein gp120 - metabolism HIV-1 - genetics HIV-1 - metabolism Humans mitochondria Mitochondria - genetics Mitochondria - metabolism Nerve Degeneration - genetics Nerve Degeneration - metabolism Nerve Degeneration - physiopathology Neurons - metabolism Neurons - pathology Up-Regulation - physiology |
| title | Mitochondria Influence Fas Expression in GP120-Induced Apoptosis of Neuronal Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-04T23%3A28%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_infor&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mitochondria%20Influence%20Fas%20Expression%20in%20GP120-Induced%20Apoptosis%20of%20Neuronal%20Cells&rft.jtitle=International%20journal%20of%20neuroscience&rft.au=Thomas,%20Sunil&rft.date=2009-01-01&rft.volume=119&rft.issue=2&rft.spage=157&rft.epage=165&rft.pages=157-165&rft.issn=0020-7454&rft.eissn=1563-5279&rft_id=info:doi/10.1080/00207450802335537&rft_dat=%3Cproquest_infor%3E66796146%3C/proquest_infor%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=66796146&rft_id=info:pmid/19125371&rfr_iscdi=true |