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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic></title><author><name sortKey="Muffat, Julien" sort="Muffat, Julien" uniqKey="Muffat J" first="Julien" last="Muffat">Julien Muffat</name><affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">University of Paris VI Pierre et Marie Curie, Paris 75006, France</nlm:aff></affiliation></author><author><name sortKey="Walker, David W" sort="Walker, David W" uniqKey="Walker D" first="David W." last="Walker">David W. Walker</name><affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff></affiliation></author><author><name sortKey="Benzer, Seymour" sort="Benzer, Seymour" uniqKey="Benzer S" first="Seymour" last="Benzer">Seymour Benzer</name><affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">18458334</idno><idno type="pmc">2374552</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374552</idno><idno type="RBID">PMC:2374552</idno><idno type="doi">10.1073/pnas.0800896105</idno><date when="2008">2008</date><idno type="wicri:Area/Pmc/Corpus">000531</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000531</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic></title><author><name sortKey="Muffat, Julien" sort="Muffat, Julien" uniqKey="Muffat J" first="Julien" last="Muffat">Julien Muffat</name><affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">University of Paris VI Pierre et Marie Curie, Paris 75006, France</nlm:aff></affiliation></author><author><name sortKey="Walker, David W" sort="Walker, David W" uniqKey="Walker D" first="David W." last="Walker">David W. Walker</name><affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff></affiliation></author><author><name sortKey="Benzer, Seymour" sort="Benzer, Seymour" uniqKey="Benzer S" first="Seymour" last="Benzer">Seymour Benzer</name><affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Apolipoprotein D (ApoD) expression increases in several neurological disorders and in spinal cord injury. We provide a report of a physiological role for human ApoD (hApoD): Flies overexpressing hApoD are long-lived and protected against stress conditions associated with aging and neurodegeneration, including hyperoxia, dietary paraquat, and heat stress. We show that the fly ortholog, <italic>Glial Lazarillo</italic>, is strongly up-regulated in response to these extrinsic stresses and also can protect <italic>in vitro</italic>-cultured cells in situations modeling Alzheimer's disease (AD) and Parkinson's disease (PD). In adult flies, hApoD overexpression reduces age-associated lipid peroxide accumulation, suggesting a proximal mechanism of action. Similar data obtained in the mouse [Ganfornina, M.D., <italic>et al.</italic>, (2008) Apolipoprotein D is involved in the mechanisms regulating protection from oxidative stress. <italic>Aging Cell</italic> 10.1111/j.1474-9726.2008.00395.] as well as in plants (Charron <italic>et al.</italic>, personal communication) suggest that ApoD and its orthologs play an evolutionarily conserved role in response to stress, possibly managing or preventing lipid peroxidation.</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">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="hwp">pnas</journal-id><journal-id journal-id-type="pmc">pnas</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title></journal-title-group><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">18458334</article-id><article-id pub-id-type="pmc">2374552</article-id><article-id pub-id-type="publisher-id">0429</article-id><article-id pub-id-type="doi">10.1073/pnas.0800896105</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Physiology</subject></subj-group></subj-group></article-categories><title-group><article-title>Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic></article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Muffat</surname><given-names>Julien</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="aff" rid="aff2"><sup>†</sup></xref><xref ref-type="corresp" rid="cor1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Walker</surname><given-names>David W.</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="corresp" rid="cor1"><sup>‡</sup></xref><xref ref-type="author-notes" rid="FN1"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Benzer</surname><given-names>Seymour</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="author-notes" rid="FN2"><sup>¶</sup></xref></contrib><aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</aff><aff id="aff2"><sup>†</sup>University of Paris VI Pierre et Marie Curie, Paris 75006, France</aff></contrib-group><author-notes><corresp id="cor1"><sup>‡</sup>To whom correspondence may be addressed. E-mail: <email>julien@caltech.edu</email> or <email>davidwalker@ucla.edu</email></corresp><fn fn-type="con"><p>Contributed by Seymour Benzer, March 26, 2008</p></fn><fn fn-type="con"><p>Author contributions: J.M., D.W.W., and S.B. designed research; J.M. performed research; J.M. contributed new reagents/analytic tools; J.M. and D.W.W. analyzed data; and J.M., D.W.W., and S.B. wrote the paper.</p></fn><fn fn-type="present-address" id="FN1"><p><sup>§</sup>Present address: Department of Physiological Science, University of California, Los Angeles, CA 90095.</p></fn><fn fn-type="deceased" id="FN2"><p><sup>¶</sup>Deceased November 30, 2007.</p></fn></author-notes><pub-date pub-type="ppub"><day>13</day><month>5</month><year>2008</year></pub-date><pub-date pub-type="epub"><day>5</day><month>5</month><year>2008</year></pub-date><pub-date pub-type="pmc-release"><day>5</day><month>5</month><year>2008</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
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<volume>105</volume><issue>19</issue><fpage>7088</fpage><lpage>7093</lpage><history><date date-type="received"><day>1</day><month>10</month><year>2007</year></date></history><permissions><copyright-statement>© 2008 by The National Academy of Sciences of the USA</copyright-statement><license license-type="open-access"><license-p>Freely available online through the PNAS open access option.</license-p></license></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zpq01908007088.pdf"></self-uri><abstract><p>Apolipoprotein D (ApoD) expression increases in several neurological disorders and in spinal cord injury. We provide a report of a physiological role for human ApoD (hApoD): Flies overexpressing hApoD are long-lived and protected against stress conditions associated with aging and neurodegeneration, including hyperoxia, dietary paraquat, and heat stress. We show that the fly ortholog, <italic>Glial Lazarillo</italic>, is strongly up-regulated in response to these extrinsic stresses and also can protect <italic>in vitro</italic>-cultured cells in situations modeling Alzheimer's disease (AD) and Parkinson's disease (PD). In adult flies, hApoD overexpression reduces age-associated lipid peroxide accumulation, suggesting a proximal mechanism of action. Similar data obtained in the mouse [Ganfornina, M.D., <italic>et al.</italic>, (2008) Apolipoprotein D is involved in the mechanisms regulating protection from oxidative stress. <italic>Aging Cell</italic> 10.1111/j.1474-9726.2008.00395.] as well as in plants (Charron <italic>et al.</italic>, personal communication) suggest that ApoD and its orthologs play an evolutionarily conserved role in response to stress, possibly managing or preventing lipid peroxidation.</p></abstract><kwd-group><kwd>aging</kwd><kwd>Alzheimer</kwd><kwd>β-amyloid</kwd><kwd>GLaz</kwd><kwd>oxidative stress</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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