Heme oxygenase-1: role in brain aging and neurodegeneration
Identifieur interne : 003494 ( Main/Exploration ); précédent : 003493; suivant : 003495Heme oxygenase-1: role in brain aging and neurodegeneration
Auteurs : H. M Schipper [Canada]Source :
- Experimental Gerontology [ 0531-5565 ] ; 2000.
Descripteurs français
- Wicri :
- topic : Fer.
English descriptors
- KwdEn :
- Aging, Alzheimer Disease (enzymology), Alzheimer Disease (pathology), Alzheimer disease, Amyloid, Animals, Astrocyte, Brain (physiology), Dopamine, Heme Oxygenase (Decyclizing) (genetics), Heme Oxygenase (Decyclizing) (physiology), Heme Oxygenase-1, Humans, Iron, Iron (metabolism), Membrane Proteins, Mitochondria, Neuroglia (metabolism), Oxidative stress, Parkinson Disease (enzymology), Parkinson disease, Rats.
- MESH :
- chemical , genetics : Heme Oxygenase (Decyclizing).
- chemical , metabolism : Iron, Neuroglia.
- enzymology : Alzheimer Disease, Parkinson Disease.
- pathology : Alzheimer Disease.
- physiology : Brain, Heme Oxygenase (Decyclizing).
- Aging, Animals, Heme Oxygenase-1, Humans, Membrane Proteins, Rats.
Abstract
The mechanisms responsible for excessive iron deposition and mitochondrial insufficiency in the aging and degenerating nervous system remain poorly understood. Heme oxygenase-1 (HO-1) is a 32kDa stress protein that degrades heme to biliverdin, free iron and carbon monoxide. Our laboratory has shown that cysteamine, dopamine, β-amyloid, IL-1β and TNF-α up-regulate HO-1 followed by mitochondrial sequestration of non-transferrin-derived 55Fe in cultured rat astroglia. In these cells and in rat astroglia transfected with the human HO-1 gene, mitochondrial iron trapping is abrogated by the HO-1 inhibitors, tin-mesoporphyrin and dexamethasone. We determined that HO-1 immunoreactivity is enhanced greatly in neurons and astrocytes of the hippocampus and cerebral cortex of Alzheimer subjects and co-localizes to senile plaques and neurofibrillary tangles (NFT). HO-1 staining is also augmented in astrocytes and decorates neuronal Lewy bodies in the Parkinson nigra. Collectively, our findings suggest that HO-1 over-expression contributes to the pathological iron deposition and mitochondrial damage documented in these aging-related neurodegenerative disorders. We recently observed that, paradoxically, HO-1 mRNA levels are markedly suppressed in peripheral lymphocytes of patients with early sporadic Alzheimer disease and may thus provide a useful biological marker of this condition.
Url:
DOI: 10.1016/S0531-5565(00)00148-0
Affiliations:
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M" last="Schipper">H. M Schipper</name><affiliation wicri:level="4"><country>Canada</country><wicri:regionArea>Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Que.</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Canada</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Gerontology</title><title level="j" type="abbrev">EXG</title><idno type="ISSN">0531-5565</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">35</biblScope><biblScope unit="issue">6–7</biblScope><biblScope unit="page" from="821">821</biblScope><biblScope unit="page" to="830">830</biblScope></imprint><idno type="ISSN">0531-5565</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0531-5565</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging</term><term>Alzheimer Disease (enzymology)</term><term>Alzheimer Disease (pathology)</term><term>Alzheimer disease</term><term>Amyloid</term><term>Animals</term><term>Astrocyte</term><term>Brain (physiology)</term><term>Dopamine</term><term>Heme Oxygenase (Decyclizing) (genetics)</term><term>Heme Oxygenase (Decyclizing) (physiology)</term><term>Heme Oxygenase-1</term><term>Humans</term><term>Iron</term><term>Iron (metabolism)</term><term>Membrane Proteins</term><term>Mitochondria</term><term>Neuroglia (metabolism)</term><term>Oxidative stress</term><term>Parkinson Disease (enzymology)</term><term>Parkinson disease</term><term>Rats</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Heme Oxygenase (Decyclizing)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Iron</term><term>Neuroglia</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Fer</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Alzheimer Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brain</term><term>Heme Oxygenase (Decyclizing)</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aging</term><term>Animals</term><term>Heme Oxygenase-1</term><term>Humans</term><term>Membrane Proteins</term><term>Rats</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mechanisms responsible for excessive iron deposition and mitochondrial insufficiency in the aging and degenerating nervous system remain poorly understood. Heme oxygenase-1 (HO-1) is a 32kDa stress protein that degrades heme to biliverdin, free iron and carbon monoxide. Our laboratory has shown that cysteamine, dopamine, β-amyloid, IL-1β and TNF-α up-regulate HO-1 followed by mitochondrial sequestration of non-transferrin-derived 55Fe in cultured rat astroglia. In these cells and in rat astroglia transfected with the human HO-1 gene, mitochondrial iron trapping is abrogated by the HO-1 inhibitors, tin-mesoporphyrin and dexamethasone. We determined that HO-1 immunoreactivity is enhanced greatly in neurons and astrocytes of the hippocampus and cerebral cortex of Alzheimer subjects and co-localizes to senile plaques and neurofibrillary tangles (NFT). HO-1 staining is also augmented in astrocytes and decorates neuronal Lewy bodies in the Parkinson nigra. Collectively, our findings suggest that HO-1 over-expression contributes to the pathological iron deposition and mitochondrial damage documented in these aging-related neurodegenerative disorders. We recently observed that, paradoxically, HO-1 mRNA levels are markedly suppressed in peripheral lymphocytes of patients with early sporadic Alzheimer disease and may thus provide a useful biological marker of this condition.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><country name="Canada"><region name="Québec"><name sortKey="Schipper, H M" sort="Schipper, H M" uniqKey="Schipper H" first="H. M" last="Schipper">H. M Schipper</name></region><name sortKey="Schipper, H M" sort="Schipper, H M" uniqKey="Schipper H" first="H. M" last="Schipper">H. M Schipper</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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