A Heme Oxygenase-1 Transducer Model of Degenerative and Developmental Brain Disorders
Identifieur interne : 000C44 ( Pmc/Curation ); précédent : 000C43; suivant : 000C45A Heme Oxygenase-1 Transducer Model of Degenerative and Developmental Brain Disorders
Auteurs : Hyman M. Schipper [Canada] ; Wei SongSource :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2015.
Abstract
Heme oxygenase-1 (HO-1) is a 32 kDa protein which catalyzes the breakdown of heme to free iron, carbon monoxide and biliverdin. The
Url:
DOI: 10.3390/ijms16035400
PubMed: 25761244
PubMed Central: 4394483
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<author><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name>
<affiliation><nlm:aff id="af1-ijms-16-05400">Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T1E2, Canada; E-Mail:<email>wsong39@yahoo.com</email>
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<affiliation wicri:level="1"><nlm:aff id="af2-ijms-16-05400">Department of Neurology & Neurosurgery and Department of Medicine, McGill University and Jewish General Hospital, Montreal, QC H3T1E2, Canada</nlm:aff>
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<wicri:regionArea>Department of Neurology & Neurosurgery and Department of Medicine, McGill University and Jewish General Hospital, Montreal, QC H3T1E2</wicri:regionArea>
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<author><name sortKey="Song, Wei" sort="Song, Wei" uniqKey="Song W" first="Wei" last="Song">Wei Song</name>
<affiliation><nlm:aff id="af1-ijms-16-05400">Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T1E2, Canada; E-Mail:<email>wsong39@yahoo.com</email>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">A Heme Oxygenase-1 Transducer Model of Degenerative and Developmental Brain Disorders</title>
<author><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name>
<affiliation><nlm:aff id="af1-ijms-16-05400">Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T1E2, Canada; E-Mail:<email>wsong39@yahoo.com</email>
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<affiliation wicri:level="1"><nlm:aff id="af2-ijms-16-05400">Department of Neurology & Neurosurgery and Department of Medicine, McGill University and Jewish General Hospital, Montreal, QC H3T1E2, Canada</nlm:aff>
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<author><name sortKey="Song, Wei" sort="Song, Wei" uniqKey="Song W" first="Wei" last="Song">Wei Song</name>
<affiliation><nlm:aff id="af1-ijms-16-05400">Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T1E2, Canada; E-Mail:<email>wsong39@yahoo.com</email>
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<series><title level="j">International Journal of Molecular Sciences</title>
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<front><div type="abstract" xml:lang="en"><p>Heme oxygenase-1 (HO-1) is a 32 kDa protein which catalyzes the breakdown of heme to free iron, carbon monoxide and biliverdin. The <italic>Hmox1</italic>
promoter contains numerous consensus sequences that render the gene exquisitely sensitive to induction by diverse pro-oxidant and inflammatory stimuli. In “stressed” astroglia, HO-1 hyperactivity promotes mitochondrial iron sequestration and macroautophagy and may thereby contribute to the pathological iron deposition and bioenergetic failure documented in Alzheimer disease, Parkinson disease and certain neurodevelopmental conditions. Glial HO-1 expression may also impact neuroplasticity and cell survival by modulating brain sterol metabolism and the proteasomal degradation of neurotoxic proteins. The glial HO-1 response may represent a pivotal transducer of noxious environmental and endogenous stressors into patterns of neural damage and repair characteristic of many human degenerative and developmental CNS disorders.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Mol Sci</journal-id>
<journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id>
<journal-id journal-id-type="publisher-id">ijms</journal-id>
<journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title>
</journal-title-group>
<issn pub-type="epub">1422-0067</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">25761244</article-id>
<article-id pub-id-type="pmc">4394483</article-id>
<article-id pub-id-type="doi">10.3390/ijms16035400</article-id>
<article-id pub-id-type="publisher-id">ijms-16-05400</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>A Heme Oxygenase-1 Transducer Model of Degenerative and Developmental Brain Disorders</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Schipper</surname>
<given-names>Hyman M.</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-16-05400">1</xref>
<xref ref-type="aff" rid="af2-ijms-16-05400">2</xref>
<xref rid="c1-ijms-16-05400" ref-type="corresp">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Song</surname>
<given-names>Wei</given-names>
</name>
<xref ref-type="aff" rid="af1-ijms-16-05400">1</xref>
</contrib>
</contrib-group>
<contrib-group><contrib contrib-type="editor"><name><surname>Harry</surname>
<given-names>G. Jean</given-names>
</name>
<role>Academic Editor</role>
</contrib>
</contrib-group>
<aff id="af1-ijms-16-05400"><label>1</label>
Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T1E2, Canada; E-Mail:<email>wsong39@yahoo.com</email>
</aff>
<aff id="af2-ijms-16-05400"><label>2</label>
Department of Neurology & Neurosurgery and Department of Medicine, McGill University and Jewish General Hospital, Montreal, QC H3T1E2, Canada</aff>
<author-notes><corresp id="c1-ijms-16-05400"><label>*</label>
Author to whom correspondence should be addressed; E-Mail: <email>hyman.schipper@mcgill.ca</email>
; Tel.: +1-514-340-8260; Fax: +1-514-340-7502.</corresp>
</author-notes>
<pub-date pub-type="epub"><day>09</day>
<month>3</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="collection"><month>3</month>
<year>2015</year>
</pub-date>
<volume>16</volume>
<issue>3</issue>
<fpage>5400</fpage>
<lpage>5419</lpage>
<history><date date-type="received"><day>11</day>
<month>12</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>22</day>
<month>2</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>© 2015 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement>
<copyright-year>2015</copyright-year>
<license><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
).</license-p>
</license>
</permissions>
<abstract><p>Heme oxygenase-1 (HO-1) is a 32 kDa protein which catalyzes the breakdown of heme to free iron, carbon monoxide and biliverdin. The <italic>Hmox1</italic>
promoter contains numerous consensus sequences that render the gene exquisitely sensitive to induction by diverse pro-oxidant and inflammatory stimuli. In “stressed” astroglia, HO-1 hyperactivity promotes mitochondrial iron sequestration and macroautophagy and may thereby contribute to the pathological iron deposition and bioenergetic failure documented in Alzheimer disease, Parkinson disease and certain neurodevelopmental conditions. Glial HO-1 expression may also impact neuroplasticity and cell survival by modulating brain sterol metabolism and the proteasomal degradation of neurotoxic proteins. The glial HO-1 response may represent a pivotal transducer of noxious environmental and endogenous stressors into patterns of neural damage and repair characteristic of many human degenerative and developmental CNS disorders.</p>
</abstract>
<kwd-group><kwd>Alzheimer disease</kwd>
<kwd>astrocyte</kwd>
<kwd>carbon monoxide</kwd>
<kwd>heme oxygenase-1</kwd>
<kwd>iron</kwd>
<kwd>macroautophagy</kwd>
<kwd>mitochondria</kwd>
<kwd>oxidative stress</kwd>
<kwd>Parkinson disease</kwd>
<kwd>schizophrenia</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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