{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360846643661798528.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/jaha.115.002485"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/JAHA.115.002485"}},{"identifier":{"@type":"PMID","@value":"26796253"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"HECT‐Type Ubiquitin E3 Ligase ITCH Interacts With Thioredoxin‐Interacting Protein and Ameliorates Reactive Oxygen Species–Induced Cardiotoxicity"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background</jats:title>\n            <jats:p xml:lang=\"en\">\n              The\n              <jats:styled-content style=\"fixed-case\">homologous to the E6‐AP carboxyl terminus (HECT)</jats:styled-content>\n              –type ubiquitin E3 ligase\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              is an enzyme that plays a pivotal role in posttranslational modification by ubiquitin proteasomal protein degradation. Thioredoxin‐interacting protein (\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              ) is a negative regulator of the thioredoxin system and an endogenous reactive oxygen species scavenger. In the present study, we focused on the functional role of ubiquitin E3 ligase\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              and its interaction with\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              to elucidate the mechanism of cardiotoxicity induced by\n              <jats:styled-content style=\"fixed-case\">reactive oxygen species</jats:styled-content>\n              , such as doxorubicin and hydrogen peroxide.\n            </jats:p>\n          </jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results</jats:title>\n            <jats:p xml:lang=\"en\">\n              Protein interaction between\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              and\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              in cardiomyocyte was confirmed by immunoprecipitation assays. Overexpression of\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              increased proteasomal\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              degradation and augmented thioredoxin activity, leading to inhibition of\n              <jats:styled-content style=\"fixed-case\">reactive oxygen species</jats:styled-content>\n              generation, p38\n              <jats:styled-content style=\"fixed-case\">MAPK</jats:styled-content>\n              , p53, and subsequent intrinsic pathway cardiomyocyte apoptosis in\n              <jats:styled-content style=\"fixed-case\">reactive oxygen species</jats:styled-content>\n              –induced cardiotoxicity. Conversely, knockdown of\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              using small interfering\n              <jats:styled-content style=\"fixed-case\">RNA</jats:styled-content>\n              inhibited\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              degradation and resulted in a subsequent increase in cardiomyocyte apoptosis. Next, we generated a transgenic mouse with cardiac‐specific overexpression of\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              , called the\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              ‐Tg mouse. The expression level of\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              in the myocardium in\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              ‐Tg mice was significantly lower than WT littermates. In\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              ‐Tg mice, cardiac dysfunction and remodeling were restored compared with WT littermates after doxorubicin injection and myocardial infarction surgery. Kaplan–Meier analysis revealed that\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              ‐Tg mice had a higher survival rate than WT littermates after doxorubicin injection and myocardial infarction surgery.\n            </jats:p>\n          </jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusion</jats:title>\n            <jats:p xml:lang=\"en\">\n              We demonstrated, for the first time, that\n              <jats:styled-content style=\"fixed-case\">ITCH</jats:styled-content>\n              targets\n              <jats:styled-content style=\"fixed-case\">TXNIP</jats:styled-content>\n              for ubiquitin‐proteasome degradation in cardiomyocytes and ameliorates\n              <jats:styled-content style=\"fixed-case\">reactive oxygen species</jats:styled-content>\n              –induced cardiotoxicity through the thioredoxin system.\n            </jats:p>\n          </jats:sec>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1420845751166599296","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"80732693"},{"@type":"NRID","@value":"1000080732693"},{"@type":"NRID","@value":"9000406228137"},{"@type":"NRID","@value":"9000405895947"},{"@type":"NRID","@value":"9000403402896"},{"@type":"NRID","@value":"9000408448466"},{"@type":"NRID","@value":"9000243885300"},{"@type":"NRID","@value":"9000309183256"},{"@type":"NRID","@value":"9000287292881"},{"@type":"NRID","@value":"9000396106292"},{"@type":"NRID","@value":"9000398639133"},{"@type":"NRID","@value":"9000018768327"},{"@type":"NRID","@value":"9000345260162"},{"@type":"NRID","@value":"9000403402855"},{"@type":"NRID","@value":"9000248246888"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/yoryoharu"}],"foaf:name":[{"@value":"Yoichiro Otaki"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513673","@type":"Researcher","foaf:name":[{"@value":"Hiroki Takahashi"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513671","@type":"Researcher","foaf:name":[{"@value":"Tetsu Watanabe"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513668","@type":"Researcher","foaf:name":[{"@value":"Akira Funayama"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513666","@type":"Researcher","foaf:name":[{"@value":"Shunsuke Netsu"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513669","@type":"Researcher","foaf:name":[{"@value":"Yuki Honda"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513667","@type":"Researcher","foaf:name":[{"@value":"Taro Narumi"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513674","@type":"Researcher","foaf:name":[{"@value":"Shinpei Kadowaki"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513676","@type":"Researcher","foaf:name":[{"@value":"Hiromasa Hasegawa"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513664","@type":"Researcher","foaf:name":[{"@value":"Shintaro Honda"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513536","@type":"Researcher","foaf:name":[{"@value":"Takanori Arimoto"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513538","@type":"Researcher","foaf:name":[{"@value":"Tetsuro Shishido"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513537","@type":"Researcher","foaf:name":[{"@value":"Takuya Miyamoto"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513672","@type":"Researcher","foaf:name":[{"@value":"Hideaki Kamata"}],"jpcoar:affiliationName":[{"@value":"Laboratory of Biomedical Chemistry, Department of Molecular Medical Science, Graduate School of Medicine, University of Hiroshima, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513675","@type":"Researcher","foaf:name":[{"@value":"Osamu Nakajima"}],"jpcoar:affiliationName":[{"@value":"Research Laboratory for Molecular Genetics, Yamagata University School of Medicine, Yamagata, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380847871938513670","@type":"Researcher","foaf:name":[{"@value":"Isao Kubota"}],"jpcoar:affiliationName":[{"@value":"Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"20479980"}],"prism:publicationName":[{"@value":"Journal of the American Heart Association"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2016-01-13","prism:volume":"5","prism:number":"1"},"reviewed":"false","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/JAHA.115.002485"}],"createdAt":"2016-01-22","modifiedAt":"2024-05-13","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Proteasome%20Endopeptidase%20Complex","dc:title":"Proteasome Endopeptidase Complex"},{"@id":"https://cir.nii.ac.jp/all?q=Time%20Factors","dc:title":"Time 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Sprague-Dawley"},{"@id":"https://cir.nii.ac.jp/all?q=Thioredoxins","dc:title":"Thioredoxins"},{"@id":"https://cir.nii.ac.jp/all?q=Diseases%20of%20the%20circulatory%20(Cardiovascular)%20system","dc:title":"Diseases of the circulatory (Cardiovascular) system"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Myocytes,%20Cardiac","dc:title":"Myocytes, Cardiac"},{"@id":"https://cir.nii.ac.jp/all?q=Cells,%20Cultured","dc:title":"Cells, Cultured"},{"@id":"https://cir.nii.ac.jp/all?q=Original%20Research","dc:title":"Original Research"},{"@id":"https://cir.nii.ac.jp/all?q=Ventricular%20Remodeling","dc:title":"Ventricular Remodeling"},{"@id":"https://cir.nii.ac.jp/all?q=Ubiquitination","dc:title":"Ubiquitination"},{"@id":"https://cir.nii.ac.jp/all?q=ITCH","dc:title":"ITCH"},{"@id":"https://cir.nii.ac.jp/all?q=thioredoxin%E2%80%90interacting%20protein","dc:title":"thioredoxin‐interacting 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of macrophage transcription factor MafB on cardiac remodeling after myocardial infarction."}]},{"@id":"https://cir.nii.ac.jp/crid/1040282257298354304","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"26893025"},{"@type":"JGN","@value":"JP26893025"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26893025/"}],"notation":[{"@language":"ja","@value":"虚血性心筋症におけるユビキチン転移酵素ITCHの機能解明"},{"@language":"en","@value":"The HECT-Type Ubiquitin E3 Ligase ITCH Interacts with Thioredoxin-Interacting Protein and Ameliorates Reactive Oxygen Species-Induced Cardiotoxicity"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050865817813692544","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@language":"en","@value":"High-mobility group box 1 restores cardiac function after myocardial infarction in transgenic 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