Contribution of the interleukin‐1β gene polymorphism in multiple system atrophy
Identifieur interne : 006536 ( Main/Merge ); précédent : 006535; suivant : 006537Contribution of the interleukin‐1β gene polymorphism in multiple system atrophy
Auteurs : Masataka Nishimura [Japon] ; Hideshi Kawakami [Japon] ; Osamu Komure [Japon] ; Hirofumi Maruyama [Japon] ; Hiroyuki Morino [Japon] ; Yuishin Izumi [Japon] ; Shigenobu Nakamura [Japon] ; Ryuji Kaji [Japon] ; Sadako Kuno [Japon]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-07.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Interleukin-1.
- genetics : Gene Frequency, Multiple System Atrophy, Polymorphism, Genetic.
- Aged, Aged, 80 and over, Alleles, Female, Genotype, Humans, Male, Middle Aged, Promoter Regions, Genetic, Reference Values.
Abstract
We studied genetic polymorphisms in the promoter region at position ‐511 of the interleukin (IL) ‐1β gene (IL‐1B‐511) and at position ‐889 of the IL‐1α gene (IL‐1A‐889), in 111 Japanese patients with multiple system atrophy (MSA) and 160 controls. The distribution of IL‐1B‐511 was significantly different between MSA patients and controls, because of the under‐representation of patients with homozygotes for allele 2 (IL‐1B‐511*2), a high producer of IL‐1β. The frequency of IL‐1A‐889*2, a high secretor of IL‐1α, was also decreased in MSA patients. Our findings suggest that abnormal cytokine expression may be implicated in the pathogenesis of MSA. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10124
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sortKey="Maruyama, Hirofumi" sort="Maruyama, Hirofumi" uniqKey="Maruyama H" first="Hirofumi" last="Maruyama">Hirofumi Maruyama</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Morino, Hiroyuki" sort="Morino, Hiroyuki" uniqKey="Morino H" first="Hiroyuki" last="Morino">Hiroyuki Morino</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Izumi, Yuishin" sort="Izumi, Yuishin" uniqKey="Izumi Y" first="Yuishin" last="Izumi">Yuishin Izumi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Nakamura, Shigenobu" sort="Nakamura, Shigenobu" uniqKey="Nakamura S" first="Shigenobu" last="Nakamura">Shigenobu Nakamura</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Kaji, Ryuji" sort="Kaji, Ryuji" uniqKey="Kaji R" first="Ryuji" last="Kaji">Ryuji Kaji</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Kuno, Sadako" sort="Kuno, Sadako" uniqKey="Kuno S" first="Sadako" last="Kuno">Sadako Kuno</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology and Clinical Research Center, Utano National Hospital, Kyoto</wicri:regionArea><wicri:noRegion>Kyoto</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-07">2002-07</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="808">808</biblScope><biblScope unit="page" to="811">811</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3A9FCA6872035A40601C18BCC37B584D7B531BAD</idno><idno type="DOI">10.1002/mds.10124</idno><idno type="ArticleID">MDS10124</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alleles</term><term>Female</term><term>Gene Frequency (genetics)</term><term>Genotype</term><term>Humans</term><term>IL‐1α</term><term>IL‐1β</term><term>Interleukin-1 (genetics)</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (genetics)</term><term>Polymorphism, Genetic (genetics)</term><term>Promoter Regions, Genetic</term><term>Reference Values</term><term>multiple system atrophy</term><term>polymorphism</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-1</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Frequency</term><term>Multiple System Atrophy</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alleles</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Promoter Regions, Genetic</term><term>Reference Values</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied genetic polymorphisms in the promoter region at position ‐511 of the interleukin (IL) ‐1β gene (IL‐1B‐511) and at position ‐889 of the IL‐1α gene (IL‐1A‐889), in 111 Japanese patients with multiple system atrophy (MSA) and 160 controls. The distribution of IL‐1B‐511 was significantly different between MSA patients and controls, because of the under‐representation of patients with homozygotes for allele 2 (IL‐1B‐511*2), a high producer of IL‐1β. The frequency of IL‐1A‐889*2, a high secretor of IL‐1α, was also decreased in MSA patients. Our findings suggest that abnormal cytokine expression may be implicated in the pathogenesis of MSA. © 2002 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.10124"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Contribution of the interleukin‐1β gene polymorphism in multiple system atrophy</title><author><name sortKey="Nishimura, Masataka" sort="Nishimura, Masataka" uniqKey="Nishimura M" first="Masataka" last="Nishimura">Masataka Nishimura</name></author><author><name sortKey="Kawakami, Hideshi" sort="Kawakami, Hideshi" uniqKey="Kawakami H" first="Hideshi" last="Kawakami">Hideshi Kawakami</name></author><author><name sortKey="Komure, Osamu" sort="Komure, Osamu" uniqKey="Komure O" first="Osamu" last="Komure">Osamu Komure</name></author><author><name sortKey="Maruyama, Hirofumi" sort="Maruyama, Hirofumi" uniqKey="Maruyama H" first="Hirofumi" last="Maruyama">Hirofumi Maruyama</name></author><author><name sortKey="Morino, Hiroyuki" sort="Morino, Hiroyuki" uniqKey="Morino H" first="Hiroyuki" last="Morino">Hiroyuki Morino</name></author><author><name sortKey="Izumi, Yuishin" sort="Izumi, Yuishin" uniqKey="Izumi Y" first="Yuishin" last="Izumi">Yuishin Izumi</name></author><author><name sortKey="Nakamura, Shigenobu" sort="Nakamura, Shigenobu" uniqKey="Nakamura S" first="Shigenobu" last="Nakamura">Shigenobu Nakamura</name></author><author><name sortKey="Kaji, Ryuji" sort="Kaji, Ryuji" uniqKey="Kaji R" first="Ryuji" last="Kaji">Ryuji Kaji</name></author><author><name sortKey="Kuno, Sadako" sort="Kuno, Sadako" uniqKey="Kuno S" first="Sadako" last="Kuno">Sadako Kuno</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:3A9FCA6872035A40601C18BCC37B584D7B531BAD</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1002/mds.10124</idno><idno type="url">https://api.istex.fr/document/3A9FCA6872035A40601C18BCC37B584D7B531BAD/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002E83</idno><idno type="wicri:Area/Istex/Curation">002E83</idno><idno type="wicri:Area/Istex/Checkpoint">002E22</idno><idno type="wicri:doubleKey">0885-3185:2002:Nishimura M:contribution:of:the</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Contribution of the interleukin‐1β gene polymorphism in multiple system atrophy</title><author><name sortKey="Nishimura, Masataka" sort="Nishimura, Masataka" uniqKey="Nishimura M" first="Masataka" last="Nishimura">Masataka Nishimura</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Kawakami, Hideshi" sort="Kawakami, Hideshi" uniqKey="Kawakami H" first="Hideshi" last="Kawakami">Hideshi Kawakami</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Komure, Osamu" sort="Komure, Osamu" uniqKey="Komure O" first="Osamu" last="Komure">Osamu Komure</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology and Clinical Research Center, Utano National Hospital, Kyoto</wicri:regionArea><wicri:noRegion>Kyoto</wicri:noRegion></affiliation></author><author><name sortKey="Maruyama, Hirofumi" sort="Maruyama, Hirofumi" uniqKey="Maruyama H" first="Hirofumi" last="Maruyama">Hirofumi Maruyama</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Morino, Hiroyuki" sort="Morino, Hiroyuki" uniqKey="Morino H" first="Hiroyuki" last="Morino">Hiroyuki Morino</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Izumi, Yuishin" sort="Izumi, Yuishin" uniqKey="Izumi Y" first="Yuishin" last="Izumi">Yuishin Izumi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Nakamura, Shigenobu" sort="Nakamura, Shigenobu" uniqKey="Nakamura S" first="Shigenobu" last="Nakamura">Shigenobu Nakamura</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Kaji, Ryuji" sort="Kaji, Ryuji" uniqKey="Kaji R" first="Ryuji" last="Kaji">Ryuji Kaji</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Kuno, Sadako" sort="Kuno, Sadako" uniqKey="Kuno S" first="Sadako" last="Kuno">Sadako Kuno</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology and Clinical Research Center, Utano National Hospital, Kyoto</wicri:regionArea><wicri:noRegion>Kyoto</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-07">2002-07</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="808">808</biblScope><biblScope unit="page" to="811">811</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3A9FCA6872035A40601C18BCC37B584D7B531BAD</idno><idno type="DOI">10.1002/mds.10124</idno><idno type="ArticleID">MDS10124</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>IL‐1α</term><term>IL‐1β</term><term>multiple system atrophy</term><term>polymorphism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied genetic polymorphisms in the promoter region at position ‐511 of the interleukin (IL) ‐1β gene (IL‐1B‐511) and at position ‐889 of the IL‐1α gene (IL‐1A‐889), in 111 Japanese patients with multiple system atrophy (MSA) and 160 controls. The distribution of IL‐1B‐511 was significantly different between MSA patients and controls, because of the under‐representation of patients with homozygotes for allele 2 (IL‐1B‐511*2), a high producer of IL‐1β. The frequency of IL‐1A‐889*2, a high secretor of IL‐1α, was also decreased in MSA patients. Our findings suggest that abnormal cytokine expression may be implicated in the pathogenesis of MSA. © 2002 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Contribution of the interleukin-1beta gene polymorphism in multiple system atrophy.</title><author><name sortKey="Nishimura, Masataka" sort="Nishimura, Masataka" uniqKey="Nishimura M" first="Masataka" last="Nishimura">Masataka Nishimura</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima, Japan. m_nishim@clin.med.tokushima-u.ac.jp</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Kawakami, Hideshi" sort="Kawakami, Hideshi" uniqKey="Kawakami H" first="Hideshi" last="Kawakami">Hideshi Kawakami</name></author><author><name sortKey="Komure, Osamu" sort="Komure, Osamu" uniqKey="Komure O" first="Osamu" last="Komure">Osamu Komure</name></author><author><name sortKey="Maruyama, Hirofumi" sort="Maruyama, Hirofumi" uniqKey="Maruyama H" first="Hirofumi" last="Maruyama">Hirofumi Maruyama</name></author><author><name sortKey="Morino, Hiroyuki" sort="Morino, Hiroyuki" uniqKey="Morino H" first="Hiroyuki" last="Morino">Hiroyuki Morino</name></author><author><name sortKey="Izumi, Yuishin" sort="Izumi, Yuishin" uniqKey="Izumi Y" first="Yuishin" last="Izumi">Yuishin Izumi</name></author><author><name sortKey="Nakamura, Shigenobu" sort="Nakamura, Shigenobu" uniqKey="Nakamura S" first="Shigenobu" last="Nakamura">Shigenobu Nakamura</name></author><author><name sortKey="Kaji, Ryuji" sort="Kaji, Ryuji" uniqKey="Kaji R" first="Ryuji" last="Kaji">Ryuji Kaji</name></author><author><name sortKey="Kuno, Sadako" sort="Kuno, Sadako" uniqKey="Kuno S" first="Sadako" last="Kuno">Sadako Kuno</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12210881</idno><idno type="pmid">12210881</idno><idno type="doi">10.1002/mds.10124</idno><idno type="wicri:Area/PubMed/Corpus">003A05</idno><idno type="wicri:Area/PubMed/Curation">003A05</idno><idno type="wicri:Area/PubMed/Checkpoint">003B52</idno><idno type="wicri:Area/Ncbi/Merge">000846</idno><idno type="wicri:Area/Ncbi/Curation">000846</idno><idno type="wicri:Area/Ncbi/Checkpoint">000846</idno><idno type="wicri:doubleKey">0885-3185:2002:Nishimura M:contribution:of:the</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Contribution of the interleukin-1beta gene polymorphism in multiple system atrophy.</title><author><name sortKey="Nishimura, Masataka" sort="Nishimura, Masataka" uniqKey="Nishimura M" first="Masataka" last="Nishimura">Masataka Nishimura</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima, Japan. m_nishim@clin.med.tokushima-u.ac.jp</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Neuroscience, Tokushima University Hospital, Tokushima</wicri:regionArea><wicri:noRegion>Tokushima</wicri:noRegion></affiliation></author><author><name sortKey="Kawakami, Hideshi" sort="Kawakami, Hideshi" uniqKey="Kawakami H" first="Hideshi" last="Kawakami">Hideshi Kawakami</name></author><author><name sortKey="Komure, Osamu" sort="Komure, Osamu" uniqKey="Komure O" first="Osamu" last="Komure">Osamu Komure</name></author><author><name sortKey="Maruyama, Hirofumi" sort="Maruyama, Hirofumi" uniqKey="Maruyama H" first="Hirofumi" last="Maruyama">Hirofumi Maruyama</name></author><author><name sortKey="Morino, Hiroyuki" sort="Morino, Hiroyuki" uniqKey="Morino H" first="Hiroyuki" last="Morino">Hiroyuki Morino</name></author><author><name sortKey="Izumi, Yuishin" sort="Izumi, Yuishin" uniqKey="Izumi Y" first="Yuishin" last="Izumi">Yuishin Izumi</name></author><author><name sortKey="Nakamura, Shigenobu" sort="Nakamura, Shigenobu" uniqKey="Nakamura S" first="Shigenobu" last="Nakamura">Shigenobu Nakamura</name></author><author><name sortKey="Kaji, Ryuji" sort="Kaji, Ryuji" uniqKey="Kaji R" first="Ryuji" last="Kaji">Ryuji Kaji</name></author><author><name sortKey="Kuno, Sadako" sort="Kuno, Sadako" uniqKey="Kuno S" first="Sadako" last="Kuno">Sadako Kuno</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alleles</term><term>Female</term><term>Gene Frequency (genetics)</term><term>Genotype</term><term>Humans</term><term>Interleukin-1 (genetics)</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (genetics)</term><term>Polymorphism, Genetic (genetics)</term><term>Promoter Regions, Genetic</term><term>Reference Values</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-1</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Frequency</term><term>Multiple System Atrophy</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alleles</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Promoter Regions, Genetic</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied genetic polymorphisms in the promoter region at position -511 of the interleukin (IL) -1beta gene (IL-1B-511) and at position -889 of the IL-1alpha gene (IL-1A-889), in 111 Japanese patients with multiple system atrophy (MSA) and 160 controls. The distribution of IL-1B-511 was significantly different between MSA patients and controls, because of the under-representation of patients with homozygotes for allele 2 (IL-1B-511*2), a high producer of IL-1beta. The frequency of IL-1A-889*2, a high secretor of IL-1alpha, was also decreased in MSA patients. Our findings suggest that abnormal cytokine expression may be implicated in the pathogenesis of MSA.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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