The Parkinson's disease gene DJ-1 is also a key regulator of stroke-induced damage.
Identifieur interne : 001032 ( PubMed/Curation ); précédent : 001031; suivant : 001033The Parkinson's disease gene DJ-1 is also a key regulator of stroke-induced damage.
Auteurs : Hossein Aleyasin [Canada] ; Maxime W C. Rousseaux ; Maryam Phillips ; Raymond H. Kim ; Ross J. Bland ; Steve Callaghan ; Ruth S. Slack ; Matthew J. During ; Tak W. Mak ; David S. ParkSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2007.
English descriptors
- KwdEn :
- Animals, Biomarkers, Brain Ischemia (metabolism), Brain Ischemia (pathology), Cells, Cultured, Cysteine (genetics), Cysteine (metabolism), Male, Mice, Mice, Knockout, Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Models, Biological, Oncogene Proteins (deficiency), Oncogene Proteins (genetics), Oncogene Proteins (metabolism), Oxidation-Reduction, Oxidative Stress, Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), Peroxiredoxins, Protein Deglycase DJ-1, Rats, Sensitivity and Specificity, Stroke (genetics), Stroke (metabolism), Stroke (pathology).
- MESH :
- chemical , deficiency : Oncogene Proteins.
- chemical , genetics : Cysteine, Microtubule-Associated Proteins, Oncogene Proteins.
- chemical , metabolism : Cysteine, Microtubule-Associated Proteins, Oncogene Proteins.
- chemical : Biomarkers, Peroxiredoxins, Protein Deglycase DJ-1.
- genetics : Parkinson Disease, Stroke.
- metabolism : Brain Ischemia, Parkinson Disease, Stroke.
- pathology : Brain Ischemia, Parkinson Disease, Stroke.
- Animals, Cells, Cultured, Male, Mice, Mice, Knockout, Models, Biological, Oxidation-Reduction, Oxidative Stress, Rats, Sensitivity and Specificity.
Abstract
Recent evidence has indicated that common mechanisms play roles among multiple neurological diseases. However, the specifics of these pathways are not completely understood. Stroke is caused by the interruption of blood flow to the brain, and cumulative evidence supports the critical role of oxidative stress in the ensuing neuronal death process. DJ-1 (PARK7) has been identified as the gene linked to early-onset familial Parkinson's disease. Currently, our work also shows that DJ-1 is central to death in both in Vitro and in Vivo models of stroke. Loss of DJ-1 increases the sensitivity to excitotoxicity and ischemia, whereas expression of DJ-1 can reverse this sensitivity and indeed provide further protection. Importantly, DJ-1 expression decreases markers of oxidative stress after stroke insult in Vivo, suggesting that DJ-1 protects through alleviation of oxidative stress. Consistent with this finding, we demonstrate the essential role of the oxidation-sensitive cysteine-106 residue in the neuroprotective activity of DJ-1 after stroke. Our work provides an important example of how a gene seemingly specific for one disease, in this case Parkinson's disease, also appears to be central in other neuropathological conditions such as stroke. It also highlights the important commonalities among differing neuropathologies.
DOI: 10.1073/pnas.0709379104
PubMed: 18003894
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pubmed:18003894Le document en format XML
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Rousseaux</name></author><author><name sortKey="Phillips, Maryam" sort="Phillips, Maryam" uniqKey="Phillips M" first="Maryam" last="Phillips">Maryam Phillips</name></author><author><name sortKey="Kim, Raymond H" sort="Kim, Raymond H" uniqKey="Kim R" first="Raymond H" last="Kim">Raymond H. Kim</name></author><author><name sortKey="Bland, Ross J" sort="Bland, Ross J" uniqKey="Bland R" first="Ross J" last="Bland">Ross J. Bland</name></author><author><name sortKey="Callaghan, Steve" sort="Callaghan, Steve" uniqKey="Callaghan S" first="Steve" last="Callaghan">Steve Callaghan</name></author><author><name sortKey="Slack, Ruth S" sort="Slack, Ruth S" uniqKey="Slack R" first="Ruth S" last="Slack">Ruth S. Slack</name></author><author><name sortKey="During, Matthew J" sort="During, Matthew J" uniqKey="During M" first="Matthew J" last="During">Matthew J. During</name></author><author><name sortKey="Mak, Tak W" sort="Mak, Tak W" uniqKey="Mak T" first="Tak W" last="Mak">Tak W. Mak</name></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S" last="Park">David S. 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Rousseaux</name></author><author><name sortKey="Phillips, Maryam" sort="Phillips, Maryam" uniqKey="Phillips M" first="Maryam" last="Phillips">Maryam Phillips</name></author><author><name sortKey="Kim, Raymond H" sort="Kim, Raymond H" uniqKey="Kim R" first="Raymond H" last="Kim">Raymond H. Kim</name></author><author><name sortKey="Bland, Ross J" sort="Bland, Ross J" uniqKey="Bland R" first="Ross J" last="Bland">Ross J. Bland</name></author><author><name sortKey="Callaghan, Steve" sort="Callaghan, Steve" uniqKey="Callaghan S" first="Steve" last="Callaghan">Steve Callaghan</name></author><author><name sortKey="Slack, Ruth S" sort="Slack, Ruth S" uniqKey="Slack R" first="Ruth S" last="Slack">Ruth S. Slack</name></author><author><name sortKey="During, Matthew J" sort="During, Matthew J" uniqKey="During M" first="Matthew J" last="During">Matthew J. During</name></author><author><name sortKey="Mak, Tak W" sort="Mak, Tak W" uniqKey="Mak T" first="Tak W" last="Mak">Tak W. Mak</name></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S" last="Park">David S. Park</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biomarkers</term><term>Brain Ischemia (metabolism)</term><term>Brain Ischemia (pathology)</term><term>Cells, Cultured</term><term>Cysteine (genetics)</term><term>Cysteine (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Knockout</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Models, Biological</term><term>Oncogene Proteins (deficiency)</term><term>Oncogene Proteins (genetics)</term><term>Oncogene Proteins (metabolism)</term><term>Oxidation-Reduction</term><term>Oxidative Stress</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Peroxiredoxins</term><term>Protein Deglycase DJ-1</term><term>Rats</term><term>Sensitivity and Specificity</term><term>Stroke (genetics)</term><term>Stroke (metabolism)</term><term>Stroke (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Oncogene Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cysteine</term><term>Microtubule-Associated Proteins</term><term>Oncogene Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cysteine</term><term>Microtubule-Associated Proteins</term><term>Oncogene Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biomarkers</term><term>Peroxiredoxins</term><term>Protein Deglycase DJ-1</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term><term>Stroke</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain Ischemia</term><term>Parkinson Disease</term><term>Stroke</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain Ischemia</term><term>Parkinson Disease</term><term>Stroke</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Male</term><term>Mice</term><term>Mice, Knockout</term><term>Models, Biological</term><term>Oxidation-Reduction</term><term>Oxidative Stress</term><term>Rats</term><term>Sensitivity and Specificity</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent evidence has indicated that common mechanisms play roles among multiple neurological diseases. However, the specifics of these pathways are not completely understood. Stroke is caused by the interruption of blood flow to the brain, and cumulative evidence supports the critical role of oxidative stress in the ensuing neuronal death process. DJ-1 (PARK7) has been identified as the gene linked to early-onset familial Parkinson's disease. Currently, our work also shows that DJ-1 is central to death in both in Vitro and in Vivo models of stroke. Loss of DJ-1 increases the sensitivity to excitotoxicity and ischemia, whereas expression of DJ-1 can reverse this sensitivity and indeed provide further protection. Importantly, DJ-1 expression decreases markers of oxidative stress after stroke insult in Vivo, suggesting that DJ-1 protects through alleviation of oxidative stress. Consistent with this finding, we demonstrate the essential role of the oxidation-sensitive cysteine-106 residue in the neuroprotective activity of DJ-1 after stroke. Our work provides an important example of how a gene seemingly specific for one disease, in this case Parkinson's disease, also appears to be central in other neuropathological conditions such as stroke. It also highlights the important commonalities among differing neuropathologies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18003894</PMID><DateCreated><Year>2007</Year><Month>11</Month><Day>27</Day></DateCreated><DateCompleted><Year>2008</Year><Month>01</Month><Day>02</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>104</Volume><Issue>47</Issue><PubDate><Year>2007</Year><Month>Nov</Month><Day>20</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>The Parkinson's disease gene DJ-1 is also a key regulator of stroke-induced damage.</ArticleTitle><Pagination><MedlinePgn>18748-53</MedlinePgn></Pagination><Abstract><AbstractText>Recent evidence has indicated that common mechanisms play roles among multiple neurological diseases. However, the specifics of these pathways are not completely understood. Stroke is caused by the interruption of blood flow to the brain, and cumulative evidence supports the critical role of oxidative stress in the ensuing neuronal death process. DJ-1 (PARK7) has been identified as the gene linked to early-onset familial Parkinson's disease. Currently, our work also shows that DJ-1 is central to death in both in Vitro and in Vivo models of stroke. Loss of DJ-1 increases the sensitivity to excitotoxicity and ischemia, whereas expression of DJ-1 can reverse this sensitivity and indeed provide further protection. Importantly, DJ-1 expression decreases markers of oxidative stress after stroke insult in Vivo, suggesting that DJ-1 protects through alleviation of oxidative stress. Consistent with this finding, we demonstrate the essential role of the oxidation-sensitive cysteine-106 residue in the neuroprotective activity of DJ-1 after stroke. Our work provides an important example of how a gene seemingly specific for one disease, in this case Parkinson's disease, also appears to be central in other neuropathological conditions such as stroke. It also highlights the important commonalities among differing neuropathologies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aleyasin</LastName><ForeName>Hossein</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Ottawa Health Research Institute, Neuroscience Group, University of Ottawa, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rousseaux</LastName><ForeName>Maxime W C</ForeName><Initials>MW</Initials></Author><Author ValidYN="Y"><LastName>Phillips</LastName><ForeName>Maryam</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Raymond H</ForeName><Initials>RH</Initials></Author><Author ValidYN="Y"><LastName>Bland</LastName><ForeName>Ross J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Callaghan</LastName><ForeName>Steve</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Slack</LastName><ForeName>Ruth S</ForeName><Initials>RS</Initials></Author><Author ValidYN="Y"><LastName>During</LastName><ForeName>Matthew J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Mak</LastName><ForeName>Tak W</ForeName><Initials>TW</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>David S</ForeName><Initials>DS</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>11</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S 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