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La maladie de Parkinson au Canada (serveur d'exploration)

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HO-1-mediated macroautophagy : a mechanism for unregulated iron deposition in aging and degenerating neural tissues

Identifieur interne : 000743 ( PascalFrancis/Curation ); précédent : 000742; suivant : 000744

HO-1-mediated macroautophagy : a mechanism for unregulated iron deposition in aging and degenerating neural tissues

Auteurs : Hillel Zukor [Canada] ; WEI SONG [Canada] ; Adrienne Liberman [Canada] ; JEANNIE MUI [Canada] ; Hojatollah Vali [Canada] ; Carine Fillebeen [Canada] ; Kostas Pantopoulos [Canada] ; Ting-Di Wu [France] ; Jean-Luc Guerquin-Kern [France] ; Hyman M. Schipper [Canada]

Source :

RBID : Pascal:09-0209855

Descripteurs français

English descriptors

Abstract

Oxidative stress, deposition of non-transferrin iron, and mitochondrial insufficiency occur in the brains of patients with Alzheimer disease (AD) and Parkinson disease (PD). We previously demonstrated that heme oxygenase-1 (HO-1) is up-regulated in AD and PD brain and promotes the accumulation of non-transferrin iron in astroglial mitochondria. Herein, dynamic secondary ion mass spectrometry (SIMS) and other techniques were employed to ascertain (i) the impact of HO-1 over-expression on astroglial mitochondrial morphology in vitro, (ii) the topography of aberrant iron sequestration in astrocytes over-expressing HO-1, and (iii) the role of iron regulatory proteins (IRP) in HO-1-mediated iron deposition. Astroglial hHO-1 over-expression induced cytoplasmic vacuolation, mitochondrial membrane damage, and macroautophagy. HO-1 promoted trapping of redox-active iron and sulfur within many cytopathological profiles without impacting ferroportin, transferrin receptor, ferritin, and IRP2 protein levels or IRP1 activity. Thus, HO-1 activity promotes mitochondrial macroautophagy and sequestration of redox-active iron in astroglia independently of classical iron mobilization pathways. Glial HO-1 may be a rational therapeutic target in AD, PD, and other human CNS conditions characterized by the unregulated deposition of brain iron.
pA  
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Pascal:09-0209855

Le document en format XML

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<title level="j" type="main">Journal of neurochemistry</title>
<title level="j" type="abbreviated">J. neurochem.</title>
<idno type="ISSN">0022-3042</idno>
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<title level="j" type="main">Journal of neurochemistry</title>
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<term>Alzheimer disease</term>
<term>Cerebral disorder</term>
<term>Dynamics</term>
<term>Encephalon</term>
<term>Heme</term>
<term>Human</term>
<term>Ions</term>
<term>Iron</term>
<term>Mass spectrometry</term>
<term>Mitochondria</term>
<term>Morphology</term>
<term>Oxidative stress</term>
<term>Parkinson disease</term>
<term>Technique</term>
<term>Transferrin</term>
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<term>Fer</term>
<term>Stress oxydatif</term>
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<term>Mitochondrie</term>
<term>Maladie de Parkinson</term>
<term>Hème</term>
<term>Encéphale</term>
<term>Dynamique</term>
<term>Pathologie de l'encéphale</term>
<term>Ion</term>
<term>Spectrométrie masse</term>
<term>Démence d'Alzheimer</term>
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<div type="abstract" xml:lang="en">Oxidative stress, deposition of non-transferrin iron, and mitochondrial insufficiency occur in the brains of patients with Alzheimer disease (AD) and Parkinson disease (PD). We previously demonstrated that heme oxygenase-1 (HO-1) is up-regulated in AD and PD brain and promotes the accumulation of non-transferrin iron in astroglial mitochondria. Herein, dynamic secondary ion mass spectrometry (SIMS) and other techniques were employed to ascertain (i) the impact of HO-1 over-expression on astroglial mitochondrial morphology in vitro, (ii) the topography of aberrant iron sequestration in astrocytes over-expressing HO-1, and (iii) the role of iron regulatory proteins (IRP) in HO-1-mediated iron deposition. Astroglial hHO-1 over-expression induced cytoplasmic vacuolation, mitochondrial membrane damage, and macroautophagy. HO-1 promoted trapping of redox-active iron and sulfur within many cytopathological profiles without impacting ferroportin, transferrin receptor, ferritin, and IRP2 protein levels or IRP1 activity. Thus, HO-1 activity promotes mitochondrial macroautophagy and sequestration of redox-active iron in astroglia independently of classical iron mobilization pathways. Glial HO-1 may be a rational therapeutic target in AD, PD, and other human CNS conditions characterized by the unregulated deposition of brain iron.</div>
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<fC03 i1="12" i2="X" l="FRE">
<s0>Démence d'Alzheimer</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Alzheimer disease</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Demencia Alzheimer</s0>
<s5>12</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Technique</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Technique</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Técnica</s0>
<s5>13</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Morphologie</s0>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Morphology</s0>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Morfología</s0>
<s5>14</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Homme</s0>
<s5>54</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG">
<s0>Human</s0>
<s5>54</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Névroglie</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Neuroglia</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Neuroglia</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>25</s5>
</fC07>
<fN21>
<s1>152</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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