Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment
Identifieur interne : 000254 ( PascalFrancis/Corpus ); précédent : 000253; suivant : 000255Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment
Auteurs : WEI SONG ; Hillel Zukor ; Shih-Hsiung Lin ; Adrienne Liberman ; Ayda Tavitian ; Jeannie Mui ; Hojatollah Vali ; Carine Fillebeen ; Kostas Pantopoulos ; Ting-Di Wu ; Jean-Luc Guerquin-Kern ; Hyman M. SchipperSource :
- Journal of neurochemistry [ 0022-3042 ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
The mechanisms responsible for pathological iron deposition in the aging and degenerating mammalian CNS remain poorly understood. The stress protein, HO-1 mediates the degradation of cellular heme to biliverdin/bilirubin, free iron, and CO and is up-regulated in the brains of persons with Alzheimer's disease and Parkinson's disease. HO-1 induction in primary astroglial cultures promotes deposition of non-transferrin iron, mitochondrial damage and macroautophagy, and predisposes cocultured neuronal elements to oxidative injury. To gain a better appreciation of the role of glial HO-1 in vivo, we probed for aberrant brain iron deposition using Perls' method and dynamic secondary ion mass spectrometry in novel, conditional GFAP.HMOX1 transgenic mice that selectively over-express human HO-1 in the astrocytic compartment. At 48 weeks, the GFAP.HMOX1 mice exhibited increased deposits of glial iron in hippocampus and other subcortical regions without overt changes in iron-regulatory and iron-binding proteins relative to age-matched wild-type animals. Dynamic secondary ion mass spectrometry revealed abundant FeO- signals in the transgenic, but not wild-type, mouse brain that colocalized to degenerate mitochondria and osmiophilic cytoplasmic inclusions (macroautophagy) documented by TEM. Sustained up-regulation of HO-1 in astrocytes promotes pathological brain iron deposition and oxidative mitochondrial damage characteristic of Alzheimer's disease-affected neural tissues. Curtailment of glial HO-1 hyperactivity may limit iron-mediated cytotoxicity in aging and degenerating neural tissues.
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Format Inist (serveur)
| NO : | FRANCIS 12-0412033 INIST |
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| ET : | Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment |
| AU : | WEI SONG; ZUKOR (Hillel); LIN (Shih-Hsiung); LIBERMAN (Adrienne); TAVITIAN (Ayda); MUI (Jeannie); VALI (Hojatollah); FILLEBEEN (Carine); PANTOPOULOS (Kostas); WU (Ting-Di); GUERQUIN-KERN (Jean-Luc); SCHIPPER (Hyman M.) |
| AF : | Lady Davis Institute, Jewish General Hospital/Montreal, Quebec/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 8 aut., 9 aut., 12 aut.); Department of Neurology and Neurosurgery, McGill University/Montreal, Quebec/Canada (2 aut., 3 aut., 5 aut., 12 aut.); Facility for Electron Microscopy Research, McGill University/Montreal, Quebec/Canada (6 aut., 7 aut.); Department of Anatomy and Cell Biolagy, Faculty of Medicine, McGill University/Montreal, Quebec/Canada (6 aut., 7 aut.); Department of Medicine, McGill University/Montreal, Quebec/Canada (9 aut.); INSERM/U759, Orsay/France (10 aut., 11 aut.); Laboratoire de Microscopie Ionique, Institut Curie/Orsay/France (10 aut., 11 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2012; Vol. 123; No. 1-2; Pp. 325-336; Bibl. 2 p. |
| LA : | Anglais |
| EA : | The mechanisms responsible for pathological iron deposition in the aging and degenerating mammalian CNS remain poorly understood. The stress protein, HO-1 mediates the degradation of cellular heme to biliverdin/bilirubin, free iron, and CO and is up-regulated in the brains of persons with Alzheimer's disease and Parkinson's disease. HO-1 induction in primary astroglial cultures promotes deposition of non-transferrin iron, mitochondrial damage and macroautophagy, and predisposes cocultured neuronal elements to oxidative injury. To gain a better appreciation of the role of glial HO-1 in vivo, we probed for aberrant brain iron deposition using Perls' method and dynamic secondary ion mass spectrometry in novel, conditional GFAP.HMOX1 transgenic mice that selectively over-express human HO-1 in the astrocytic compartment. At 48 weeks, the GFAP.HMOX1 mice exhibited increased deposits of glial iron in hippocampus and other subcortical regions without overt changes in iron-regulatory and iron-binding proteins relative to age-matched wild-type animals. Dynamic secondary ion mass spectrometry revealed abundant FeO- signals in the transgenic, but not wild-type, mouse brain that colocalized to degenerate mitochondria and osmiophilic cytoplasmic inclusions (macroautophagy) documented by TEM. Sustained up-regulation of HO-1 in astrocytes promotes pathological brain iron deposition and oxidative mitochondrial damage characteristic of Alzheimer's disease-affected neural tissues. Curtailment of glial HO-1 hyperactivity may limit iron-mediated cytotoxicity in aging and degenerating neural tissues. |
| CC : | 770D03M |
| FD : | Encéphale; Fer; Système nerveux central; Stress; Protéine liaison; Hème; Induction; Culture primaire; Démence d'Alzheimer; Transferrine; Mitochondrie; Maladie de Parkinson; Méthode dynamique; Ion; Souris; Homme |
| FG : | Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux; Syndrome extrapyramidal; Névroglie; Rodentia; Mammalia; Vertebrata |
| ED : | Encephalon; Iron; Central nervous system; Stress; Binding protein; Heme; Induction; Primary culture; Alzheimer disease; Transferrin; Mitochondria; Parkinson disease; Dynamic method; Ions; Mouse; Human |
| EG : | Cerebral disorder; Degenerative disease; Central nervous system disease; Nervous system diseases; Extrapyramidal syndrome; Neuroglia; Rodentia; Mammalia; Vertebrata |
| SD : | Encéfalo; Hierro; Sistema nervioso central; Estrés; Proteína enlace; Heme; Inducción; Cultivo primario; Demencia Alzheimer; Transferrina; Mitocondria; Parkinson enfermedad; Método dinámico; Ión; Ratón; Hombre |
| LO : | INIST-4037.354000506820050290 |
| ID : | 12-0412033 |
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aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fillebeen, Carine" sort="Fillebeen, Carine" uniqKey="Fillebeen C" first="Carine" last="Fillebeen">Carine Fillebeen</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Pantopoulos, Kostas" sort="Pantopoulos, Kostas" uniqKey="Pantopoulos K" first="Kostas" last="Pantopoulos">Kostas Pantopoulos</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Department of Medicine, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Wu, Ting Di" sort="Wu, Ting Di" uniqKey="Wu T" first="Ting-Di" last="Wu">Ting-Di Wu</name><affiliation><inist:fA14 i1="06"><s1>INSERM</s1><s2>U759, Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="07"><s1>Laboratoire de Microscopie Ionique, Institut Curie</s1><s2>Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Guerquin Kern, Jean Luc" sort="Guerquin Kern, Jean Luc" uniqKey="Guerquin Kern J" first="Jean-Luc" last="Guerquin-Kern">Jean-Luc Guerquin-Kern</name><affiliation><inist:fA14 i1="06"><s1>INSERM</s1><s2>U759, Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="07"><s1>Laboratoire de Microscopie Ionique, Institut Curie</s1><s2>Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Neurology and Neurosurgery, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0412033</idno><date when="2012">2012</date><idno type="stanalyst">FRANCIS 12-0412033 INIST</idno><idno type="RBID">Francis:12-0412033</idno><idno type="wicri:Area/PascalFrancis/Corpus">000254</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment</title><author><name sortKey="Wei Song" sort="Wei Song" uniqKey="Wei Song" last="Wei Song">WEI SONG</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Zukor, Hillel" sort="Zukor, Hillel" uniqKey="Zukor H" first="Hillel" last="Zukor">Hillel Zukor</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Neurology and Neurosurgery, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lin, Shih Hsiung" sort="Lin, Shih Hsiung" uniqKey="Lin S" first="Shih-Hsiung" last="Lin">Shih-Hsiung Lin</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Neurology and Neurosurgery, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Liberman, Adrienne" sort="Liberman, Adrienne" uniqKey="Liberman A" first="Adrienne" last="Liberman">Adrienne Liberman</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Tavitian, Ayda" sort="Tavitian, Ayda" uniqKey="Tavitian A" first="Ayda" last="Tavitian">Ayda Tavitian</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Neurology and Neurosurgery, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Mui, Jeannie" sort="Mui, Jeannie" uniqKey="Mui J" first="Jeannie" last="Mui">Jeannie Mui</name><affiliation><inist:fA14 i1="03"><s1>Facility for Electron Microscopy Research, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Anatomy and Cell Biolagy, Faculty of Medicine, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Vali, Hojatollah" sort="Vali, Hojatollah" uniqKey="Vali H" first="Hojatollah" last="Vali">Hojatollah Vali</name><affiliation><inist:fA14 i1="03"><s1>Facility for Electron Microscopy Research, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Anatomy and Cell Biolagy, Faculty of Medicine, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fillebeen, Carine" sort="Fillebeen, Carine" uniqKey="Fillebeen C" first="Carine" last="Fillebeen">Carine Fillebeen</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Pantopoulos, Kostas" sort="Pantopoulos, Kostas" uniqKey="Pantopoulos K" first="Kostas" last="Pantopoulos">Kostas Pantopoulos</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Department of Medicine, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Wu, Ting Di" sort="Wu, Ting Di" uniqKey="Wu T" first="Ting-Di" last="Wu">Ting-Di Wu</name><affiliation><inist:fA14 i1="06"><s1>INSERM</s1><s2>U759, Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="07"><s1>Laboratoire de Microscopie Ionique, Institut Curie</s1><s2>Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Guerquin Kern, Jean Luc" sort="Guerquin Kern, Jean Luc" uniqKey="Guerquin Kern J" first="Jean-Luc" last="Guerquin-Kern">Jean-Luc Guerquin-Kern</name><affiliation><inist:fA14 i1="06"><s1>INSERM</s1><s2>U759, Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="07"><s1>Laboratoire de Microscopie Ionique, Institut Curie</s1><s2>Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name><affiliation><inist:fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Neurology and Neurosurgery, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer disease</term><term>Binding protein</term><term>Central nervous system</term><term>Dynamic method</term><term>Encephalon</term><term>Heme</term><term>Human</term><term>Induction</term><term>Ions</term><term>Iron</term><term>Mitochondria</term><term>Mouse</term><term>Parkinson disease</term><term>Primary culture</term><term>Stress</term><term>Transferrin</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Encéphale</term><term>Fer</term><term>Système nerveux central</term><term>Stress</term><term>Protéine liaison</term><term>Hème</term><term>Induction</term><term>Culture primaire</term><term>Démence d'Alzheimer</term><term>Transferrine</term><term>Mitochondrie</term><term>Maladie de Parkinson</term><term>Méthode dynamique</term><term>Ion</term><term>Souris</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mechanisms responsible for pathological iron deposition in the aging and degenerating mammalian CNS remain poorly understood. The stress protein, HO-1 mediates the degradation of cellular heme to biliverdin/bilirubin, free iron, and CO and is up-regulated in the brains of persons with Alzheimer's disease and Parkinson's disease. HO-1 induction in primary astroglial cultures promotes deposition of non-transferrin iron, mitochondrial damage and macroautophagy, and predisposes cocultured neuronal elements to oxidative injury. To gain a better appreciation of the role of glial HO-1 in vivo, we probed for aberrant brain iron deposition using Perls' method and dynamic secondary ion mass spectrometry in novel, conditional GFAP.HMOX1 transgenic mice that selectively over-express human HO-1 in the astrocytic compartment. At 48 weeks, the GFAP.HMOX1 mice exhibited increased deposits of glial iron in hippocampus and other subcortical regions without overt changes in iron-regulatory and iron-binding proteins relative to age-matched wild-type animals. Dynamic secondary ion mass spectrometry revealed abundant FeO<sup>-</sup> signals in the transgenic, but not wild-type, mouse brain that colocalized to degenerate mitochondria and osmiophilic cytoplasmic inclusions (macroautophagy) documented by TEM. Sustained up-regulation of HO-1 in astrocytes promotes pathological brain iron deposition and oxidative mitochondrial damage characteristic of Alzheimer's disease-affected neural tissues. Curtailment of glial HO-1 hyperactivity may limit iron-mediated cytotoxicity in aging and degenerating neural tissues.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>123</s2></fA05><fA06><s2>1-2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment</s1></fA08><fA11 i1="01" i2="1"><s1>WEI SONG</s1></fA11><fA11 i1="02" i2="1"><s1>ZUKOR (Hillel)</s1></fA11><fA11 i1="03" i2="1"><s1>LIN (Shih-Hsiung)</s1></fA11><fA11 i1="04" i2="1"><s1>LIBERMAN (Adrienne)</s1></fA11><fA11 i1="05" i2="1"><s1>TAVITIAN (Ayda)</s1></fA11><fA11 i1="06" i2="1"><s1>MUI (Jeannie)</s1></fA11><fA11 i1="07" i2="1"><s1>VALI (Hojatollah)</s1></fA11><fA11 i1="08" i2="1"><s1>FILLEBEEN (Carine)</s1></fA11><fA11 i1="09" i2="1"><s1>PANTOPOULOS (Kostas)</s1></fA11><fA11 i1="10" i2="1"><s1>WU (Ting-Di)</s1></fA11><fA11 i1="11" i2="1"><s1>GUERQUIN-KERN (Jean-Luc)</s1></fA11><fA11 i1="12" i2="1"><s1>SCHIPPER (Hyman M.)</s1></fA11><fA14 i1="01"><s1>Lady Davis Institute, Jewish General Hospital</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Neurology and Neurosurgery, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="03"><s1>Facility for Electron Microscopy Research, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Anatomy and Cell Biolagy, Faculty of Medicine, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Medicine, McGill University</s1><s2>Montreal, Quebec</s2><s3>CAN</s3><sZ>9 aut.</sZ></fA14><fA14 i1="06"><s1>INSERM</s1><s2>U759, Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></fA14><fA14 i1="07"><s1>Laboratoire de Microscopie Ionique, Institut Curie</s1><s2>Orsay</s2><s3>FRA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></fA14><fA20><s1>325-336</s1></fA20><fA21><s1>2012</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000506820050290</s5></fA43><fA44><s0>0000</s0><s1>© 2012 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>2 p.</s0></fA45><fA47 i1="01" i2="1"><s0>12-0412033</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>The mechanisms responsible for pathological iron deposition in the aging and degenerating mammalian CNS remain poorly understood. The stress protein, HO-1 mediates the degradation of cellular heme to biliverdin/bilirubin, free iron, and CO and is up-regulated in the brains of persons with Alzheimer's disease and Parkinson's disease. HO-1 induction in primary astroglial cultures promotes deposition of non-transferrin iron, mitochondrial damage and macroautophagy, and predisposes cocultured neuronal elements to oxidative injury. To gain a better appreciation of the role of glial HO-1 in vivo, we probed for aberrant brain iron deposition using Perls' method and dynamic secondary ion mass spectrometry in novel, conditional GFAP.HMOX1 transgenic mice that selectively over-express human HO-1 in the astrocytic compartment. At 48 weeks, the GFAP.HMOX1 mice exhibited increased deposits of glial iron in hippocampus and other subcortical regions without overt changes in iron-regulatory and iron-binding proteins relative to age-matched wild-type animals. Dynamic secondary ion mass spectrometry revealed abundant FeO<sup>-</sup> signals in the transgenic, but not wild-type, mouse brain that colocalized to degenerate mitochondria and osmiophilic cytoplasmic inclusions (macroautophagy) documented by TEM. Sustained up-regulation of HO-1 in astrocytes promotes pathological brain iron deposition and oxidative mitochondrial damage characteristic of Alzheimer's disease-affected neural tissues. Curtailment of glial HO-1 hyperactivity may limit iron-mediated cytotoxicity in aging and degenerating neural tissues.</s0></fC01><fC02 i1="01" i2="X"><s0>770D03M</s0><s1>IV</s1></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Encéphale</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Encephalon</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Encéfalo</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Fer</s0><s2>NC</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Iron</s0><s2>NC</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Hierro</s0><s2>NC</s2><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Central nervous system</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Stress</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Stress</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Estrés</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Protéine liaison</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Binding protein</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Proteína enlace</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Hème</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Heme</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Heme</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Induction</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Induction</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Inducción</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Culture primaire</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Primary culture</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Cultivo primario</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Démence d'Alzheimer</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Alzheimer disease</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Demencia Alzheimer</s0><s5>09</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Transferrine</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Transferrin</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Transferrina</s0><s5>10</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Mitochondrie</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Mitochondria</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Mitocondria</s0><s5>11</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>12</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>12</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>12</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Méthode dynamique</s0><s5>13</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Dynamic method</s0><s5>13</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Método dinámico</s0><s5>13</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Ion</s0><s2>NA</s2><s5>14</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Ions</s0><s2>NA</s2><s5>14</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Ión</s0><s2>NA</s2><s5>14</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Souris</s0><s5>54</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Mouse</s0><s5>54</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Ratón</s0><s5>54</s5></fC03><fC03 i1="16" i2="X" l="FRE"><s0>Homme</s0><s5>55</s5></fC03><fC03 i1="16" i2="X" l="ENG"><s0>Human</s0><s5>55</s5></fC03><fC03 i1="16" i2="X" l="SPA"><s0>Hombre</s0><s5>55</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>20</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>20</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>20</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>21</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>21</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>21</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>22</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>22</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>22</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>23</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>23</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>23</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>24</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>24</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>24</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Névroglie</s0><s5>25</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Neuroglia</s0><s5>25</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Neuroglia</s0><s5>25</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>317</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>FRANCIS 12-0412033 INIST</NO><ET>Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment</ET><AU>WEI SONG; ZUKOR (Hillel); LIN (Shih-Hsiung); LIBERMAN (Adrienne); TAVITIAN (Ayda); MUI (Jeannie); VALI (Hojatollah); FILLEBEEN (Carine); PANTOPOULOS (Kostas); WU (Ting-Di); GUERQUIN-KERN (Jean-Luc); SCHIPPER (Hyman M.)</AU><AF>Lady Davis Institute, Jewish General Hospital/Montreal, Quebec/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 8 aut., 9 aut., 12 aut.); Department of Neurology and Neurosurgery, McGill University/Montreal, Quebec/Canada (2 aut., 3 aut., 5 aut., 12 aut.); Facility for Electron Microscopy Research, McGill University/Montreal, Quebec/Canada (6 aut., 7 aut.); Department of Anatomy and Cell Biolagy, Faculty of Medicine, McGill University/Montreal, Quebec/Canada (6 aut., 7 aut.); Department of Medicine, McGill University/Montreal, Quebec/Canada (9 aut.); INSERM/U759, Orsay/France (10 aut., 11 aut.); Laboratoire de Microscopie Ionique, Institut Curie/Orsay/France (10 aut., 11 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2012; Vol. 123; No. 1-2; Pp. 325-336; Bibl. 2 p.</SO><LA>Anglais</LA><EA>The mechanisms responsible for pathological iron deposition in the aging and degenerating mammalian CNS remain poorly understood. The stress protein, HO-1 mediates the degradation of cellular heme to biliverdin/bilirubin, free iron, and CO and is up-regulated in the brains of persons with Alzheimer's disease and Parkinson's disease. HO-1 induction in primary astroglial cultures promotes deposition of non-transferrin iron, mitochondrial damage and macroautophagy, and predisposes cocultured neuronal elements to oxidative injury. To gain a better appreciation of the role of glial HO-1 in vivo, we probed for aberrant brain iron deposition using Perls' method and dynamic secondary ion mass spectrometry in novel, conditional GFAP.HMOX1 transgenic mice that selectively over-express human HO-1 in the astrocytic compartment. At 48 weeks, the GFAP.HMOX1 mice exhibited increased deposits of glial iron in hippocampus and other subcortical regions without overt changes in iron-regulatory and iron-binding proteins relative to age-matched wild-type animals. Dynamic secondary ion mass spectrometry revealed abundant FeO<sup>-</sup> signals in the transgenic, but not wild-type, mouse brain that colocalized to degenerate mitochondria and osmiophilic cytoplasmic inclusions (macroautophagy) documented by TEM. Sustained up-regulation of HO-1 in astrocytes promotes pathological brain iron deposition and oxidative mitochondrial damage characteristic of Alzheimer's disease-affected neural tissues. Curtailment of glial HO-1 hyperactivity may limit iron-mediated cytotoxicity in aging and degenerating neural tissues.</EA><CC>770D03M</CC><FD>Encéphale; Fer; Système nerveux central; Stress; Protéine liaison; Hème; Induction; Culture primaire; Démence d'Alzheimer; Transferrine; Mitochondrie; Maladie de Parkinson; Méthode dynamique; Ion; Souris; Homme</FD><FG>Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux; Syndrome extrapyramidal; Névroglie; Rodentia; Mammalia; Vertebrata</FG><ED>Encephalon; Iron; Central nervous system; Stress; Binding protein; Heme; Induction; Primary culture; Alzheimer disease; Transferrin; Mitochondria; Parkinson disease; Dynamic method; Ions; Mouse; Human</ED><EG>Cerebral disorder; Degenerative disease; Central nervous system disease; Nervous system diseases; Extrapyramidal syndrome; Neuroglia; Rodentia; Mammalia; Vertebrata</EG><SD>Encéfalo; Hierro; Sistema nervioso central; Estrés; Proteína enlace; Heme; Inducción; Cultivo primario; Demencia Alzheimer; Transferrina; Mitocondria; Parkinson enfermedad; Método dinámico; Ión; Ratón; Hombre</SD><LO>INIST-4037.354000506820050290</LO><ID>12-0412033</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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