ParkinsonFranceV1, Ncbi, Merge, bibRecord, 000856

Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in Drosophila

Identifieur interne : 000856 ( Ncbi/Merge ); précédent : 000855; suivant : 000857

Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in Drosophila

Auteurs : Julien Muffat [États-Unis, France] ; David W. Walker [États-Unis] ; Seymour Benzer [États-Unis]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2008.

RBID : PMC:2374552

Abstract

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, Glial Lazarillo, is strongly up-regulated in response to these extrinsic stresses and also can protect in vitro-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., et al., (2008) Apolipoprotein D is involved in the mechanisms regulating protection from oxidative stress. Aging Cell 10.1111/j.1474-9726.2008.00395.] as well as in plants (Charron et al., personal communication) suggest that ApoD and its orthologs play an evolutionarily conserved role in response to stress, possibly managing or preventing lipid peroxidation.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374552

DOI: 10.1073/pnas.0800896105
PubMed: 18458334
PubMed Central: 2374552

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PMC:2374552

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<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>
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<title-group><article-title>Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic>
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<contrib-group><contrib contrib-type="author"><name><surname>Muffat</surname>
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<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="aff" rid="aff2"><sup>†</sup>
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<aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</aff>
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University of Paris VI Pierre et Marie Curie, Paris 75006, France</aff>
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<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>
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<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>
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Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in Drosophila

Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in Drosophila

Source :

Abstract

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