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

Identifieur interne : 002508 ( Main/Merge ); précédent : 002507; suivant : 002509

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

Le document en format XML

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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>
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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

Links toward previous steps (curation, corpus...)

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Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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Pour générer des pages wiki