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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Deregulation of microRNAs by HIV-1 Vpr Protein Leads to the Development of Neurocognitive Disorders<xref ref-type="fn" rid="FN1">*</xref></title><author><name sortKey="Mukerjee, Ruma" sort="Mukerjee, Ruma" uniqKey="Mukerjee R" first="Ruma" last="Mukerjee">Ruma Mukerjee</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Chang, J Robert" sort="Chang, J Robert" uniqKey="Chang J" first="J. Robert" last="Chang">J. Robert Chang</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Del Valle, Luis" sort="Del Valle, Luis" uniqKey="Del Valle L" first="Luis" last="Del Valle">Luis Del Valle</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Bagashev, Asen" sort="Bagashev, Asen" uniqKey="Bagashev A" first="Asen" last="Bagashev">Asen Bagashev</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Gayed, Monika M" sort="Gayed, Monika M" uniqKey="Gayed M" first="Monika M." last="Gayed">Monika M. Gayed</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Lyde, Randolph B" sort="Lyde, Randolph B" uniqKey="Lyde R" first="Randolph B." last="Lyde">Randolph B. Lyde</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hawkins, Brian J" sort="Hawkins, Brian J" uniqKey="Hawkins B" first="Brian J." last="Hawkins">Brian J. Hawkins</name><affiliation><nlm:aff id="aff4">Anesthesiology and Pain Medicine, Mitochondria and Metabolism Center, University of Washington, Seattle, Washington 98109,</nlm:aff></affiliation></author><author><name sortKey="Brailoiu, Eugen" sort="Brailoiu, Eugen" uniqKey="Brailoiu E" first="Eugen" last="Brailoiu">Eugen Brailoiu</name><affiliation><nlm:aff id="aff2">Pharmacology, Molecular Studies of Neurodegenerative Diseases Laboratory, Temple University School of Medicine, Philadelphia, Pennsylvania 19140,</nlm:aff></affiliation></author><author><name sortKey="Cohen, Eric" sort="Cohen, Eric" uniqKey="Cohen E" first="Eric" last="Cohen">Eric Cohen</name><affiliation><nlm:aff id="aff5"></nlm:aff></affiliation></author><author><name sortKey="Power, Chris" sort="Power, Chris" uniqKey="Power C" first="Chris" last="Power">Chris Power</name><affiliation><nlm:aff id="aff6"></nlm:aff></affiliation></author><author><name sortKey="Azizi, S Ausim" sort="Azizi, S Ausim" uniqKey="Azizi S" first="S. Ausim" last="Azizi">S. Ausim Azizi</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Gelman, Benjamin B" sort="Gelman, Benjamin B" uniqKey="Gelman B" first="Benjamin B." last="Gelman">Benjamin B. Gelman</name><affiliation><nlm:aff id="aff7"></nlm:aff></affiliation></author><author><name sortKey="Sawaya, Bassel E" sort="Sawaya, Bassel E" uniqKey="Sawaya B" first="Bassel E." last="Sawaya">Bassel E. Sawaya</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21816823</idno><idno type="pmc">3186354</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3186354</idno><idno type="RBID">PMC:3186354</idno><idno type="doi">10.1074/jbc.M111.241547</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000560</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000560</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Deregulation of microRNAs by HIV-1 Vpr Protein Leads to the Development of Neurocognitive Disorders<xref ref-type="fn" rid="FN1">*</xref></title><author><name sortKey="Mukerjee, Ruma" sort="Mukerjee, Ruma" uniqKey="Mukerjee R" first="Ruma" last="Mukerjee">Ruma Mukerjee</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Chang, J Robert" sort="Chang, J Robert" uniqKey="Chang J" first="J. Robert" last="Chang">J. Robert Chang</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Del Valle, Luis" sort="Del Valle, Luis" uniqKey="Del Valle L" first="Luis" last="Del Valle">Luis Del Valle</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Bagashev, Asen" sort="Bagashev, Asen" uniqKey="Bagashev A" first="Asen" last="Bagashev">Asen Bagashev</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Gayed, Monika M" sort="Gayed, Monika M" uniqKey="Gayed M" first="Monika M." last="Gayed">Monika M. Gayed</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Lyde, Randolph B" sort="Lyde, Randolph B" uniqKey="Lyde R" first="Randolph B." last="Lyde">Randolph B. Lyde</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hawkins, Brian J" sort="Hawkins, Brian J" uniqKey="Hawkins B" first="Brian J." last="Hawkins">Brian J. Hawkins</name><affiliation><nlm:aff id="aff4">Anesthesiology and Pain Medicine, Mitochondria and Metabolism Center, University of Washington, Seattle, Washington 98109,</nlm:aff></affiliation></author><author><name sortKey="Brailoiu, Eugen" sort="Brailoiu, Eugen" uniqKey="Brailoiu E" first="Eugen" last="Brailoiu">Eugen Brailoiu</name><affiliation><nlm:aff id="aff2">Pharmacology, Molecular Studies of Neurodegenerative Diseases Laboratory, Temple University School of Medicine, Philadelphia, Pennsylvania 19140,</nlm:aff></affiliation></author><author><name sortKey="Cohen, Eric" sort="Cohen, Eric" uniqKey="Cohen E" first="Eric" last="Cohen">Eric Cohen</name><affiliation><nlm:aff id="aff5"></nlm:aff></affiliation></author><author><name sortKey="Power, Chris" sort="Power, Chris" uniqKey="Power C" first="Chris" last="Power">Chris Power</name><affiliation><nlm:aff id="aff6"></nlm:aff></affiliation></author><author><name sortKey="Azizi, S Ausim" sort="Azizi, S Ausim" uniqKey="Azizi S" first="S. Ausim" last="Azizi">S. Ausim Azizi</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Gelman, Benjamin B" sort="Gelman, Benjamin B" uniqKey="Gelman B" first="Benjamin B." last="Gelman">Benjamin B. Gelman</name><affiliation><nlm:aff id="aff7"></nlm:aff></affiliation></author><author><name sortKey="Sawaya, Bassel E" sort="Sawaya, Bassel E" uniqKey="Sawaya B" first="Bassel E." last="Sawaya">Bassel E. Sawaya</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">The Journal of Biological Chemistry</title><idno type="ISSN">0021-9258</idno><idno type="eISSN">1083-351X</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and <italic>v</italic>- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (<italic>e.g.</italic> miR-34a) and their target genes (<italic>e.g.</italic> CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Biol Chem</journal-id><journal-id journal-id-type="hwp">jbc</journal-id><journal-id journal-id-type="pmc">jbc</journal-id><journal-id journal-id-type="publisher-id">JBC</journal-id><journal-title-group><journal-title>The Journal of Biological Chemistry</journal-title></journal-title-group><issn pub-type="ppub">0021-9258</issn><issn pub-type="epub">1083-351X</issn><publisher><publisher-name>American Society for Biochemistry and Molecular Biology</publisher-name><publisher-loc>9650 Rockville Pike, Bethesda, MD 20814, U.S.A.</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">21816823</article-id><article-id pub-id-type="pmc">3186354</article-id><article-id pub-id-type="publisher-id">M111.241547</article-id><article-id pub-id-type="doi">10.1074/jbc.M111.241547</article-id><article-categories><subj-group subj-group-type="heading"><subject>Molecular Bases of Disease</subject></subj-group></article-categories><title-group><article-title>Deregulation of microRNAs by HIV-1 Vpr Protein Leads to the Development of Neurocognitive Disorders<xref ref-type="fn" rid="FN1">*</xref></article-title><alt-title alt-title-type="short">Involvement of Vpr in HAND</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Mukerjee</surname><given-names>Ruma</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Chang</surname><given-names>J. Robert</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Del Valle</surname><given-names>Luis</given-names></name><xref ref-type="aff" rid="aff3"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bagashev</surname><given-names>Asen</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Gayed</surname><given-names>Monika M.</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lyde</surname><given-names>Randolph B.</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hawkins</surname><given-names>Brian J.</given-names></name><xref ref-type="aff" rid="aff4"><sup>¶</sup></xref></contrib><contrib contrib-type="author"><name><surname>Brailoiu</surname><given-names>Eugen</given-names></name><xref ref-type="aff" rid="aff2"><sup>‖</sup></xref></contrib><contrib contrib-type="author"><name><surname>Cohen</surname><given-names>Eric</given-names></name><xref ref-type="aff" rid="aff5">**</xref></contrib><contrib contrib-type="author"><name><surname>Power</surname><given-names>Chris</given-names></name><xref ref-type="aff" rid="aff6"><sup>‡‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Azizi</surname><given-names>S. Ausim</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Gelman</surname><given-names>Benjamin B.</given-names></name><xref ref-type="aff" rid="aff7"><sup>§§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sawaya</surname><given-names>Bassel E.</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff id="aff1">From the Departments of<label>‡</label>Neurology, and</aff><aff id="aff2"><label>‖</label>Pharmacology, Molecular Studies of Neurodegenerative Diseases Laboratory, Temple University School of Medicine, Philadelphia, Pennsylvania 19140,</aff><aff id="aff3">the<label>§</label>Department of Medicine, Section of Hematology/Oncology, and Department of Pathology, Stanley S. Scott Cancer Center, Louisiana State University School of Medicine, New Orleans, Louisiana 70112,</aff><aff id="aff4"><label>¶</label>Anesthesiology and Pain Medicine, Mitochondria and Metabolism Center, University of Washington, Seattle, Washington 98109,</aff><aff id="aff5">the<label>**</label>Institut de Recherches Cliniques de Montréal (IRCM) and Department of Microbiology and Immunology, Université de Montréal, Quebec, Canada,</aff><aff id="aff6">the<label>‡‡</label>Departments of Medicine (Neurology), Medical Microbiology & Immunology, and Psychiatry, University of Alberta, Edmonton, Alberta T6G 2S2, Canada, and</aff><aff id="aff7">the<label>§§</label>Departments of Pathology and Neuroscience & Cell Biology, Texas NeuroAIDS Research Center, University of Texas Medical Branch, Galveston, Texas 77555-0609</aff></contrib-group><author-notes><corresp id="cor1"><label>1</label> To whom correspondence should be addressed: <addr-line>Molecular Studies of Neurodegenerative Diseases Lab, 3420 North Broad Street, MRB 719; Philadelphia, PA 19140.</addr-line> Tel.: <phone>215-707-5446</phone>; Fax: <fax>215-707-5948</fax>; E-mail: <email>sawaya@temple.edu</email>.</corresp></author-notes><pub-date pub-type="ppub"><day>7</day><month>10</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>4</day><month>8</month><year>2011</year></pub-date><volume>286</volume><issue>40</issue><fpage>34976</fpage><lpage>34985</lpage><history><date date-type="received"><day>21</day><month>3</month><year>2011</year></date><date date-type="rev-recd"><day>2</day><month>8</month><year>2011</year></date></history><permissions><copyright-statement>© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.</copyright-statement><copyright-year>2011</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zbc04011034976.pdf"></self-uri><abstract><p>Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and <italic>v</italic>- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (<italic>e.g.</italic> miR-34a) and their target genes (<italic>e.g.</italic> CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders.</p></abstract><kwd-group><kwd>Calcium</kwd><kwd>Endoplasmic Reticulum (ER)</kwd><kwd>HIV</kwd><kwd>MicroRNA</kwd><kwd>Mitochondria</kwd><kwd>Neurodegeneration</kwd></kwd-group><funding-group><award-group><funding-source id="CS100">National Institutes of Health</funding-source><award-id rid="CS100">R01-NS059327</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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