The Role of/SUMO-1 in Cardiac Oxidative Stress and Hypertrophy
DC Field | Value | Language |
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dc.contributor.author | Lee, Ahyoung | - |
dc.contributor.author | Jeong, Dongtak | - |
dc.contributor.author | Mitsuyama, Shinichi | - |
dc.contributor.author | Kho, Changwon | - |
dc.contributor.author | Hajjar, Roger J. | - |
dc.date.accessioned | 2021-06-23T02:03:43Z | - |
dc.date.available | 2021-06-23T02:03:43Z | - |
dc.date.issued | 2013-11 | - |
dc.identifier.issn | 0009-7322 | - |
dc.identifier.issn | 1524-4539 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/26296 | - |
dc.description.abstract | Background: Small ubiquitin-like modifier type 1 (SUMO-1) has been shown to have a critical role in the dysfunction of the cardiac isoform of the sarcoplasmic reticulum calcium ATPase pump (SERCA2a) in the setting of heart failure. In cardiac hypertrophy the role of SUMO-1 has not been defined and our study’s goals were to examine the effects of modulating SUMO-1 on the hypertrophic response in vitro and in vivo and to examine whether oxidative stress (during cardiac hypertrophy) is abrogated by SUMO-1 gene transfer. Results: In mice undergoing trans-aortic constriction (TAC), SUMO-1 levels increased slightly during the compensated stage of hypertrophy and then dropped sharply following the transition to heart failure. In isolated cardiomyocytes, SUMO-1 gene transfer inhibited hypertrophic responses in the presence of phenylephrine. AAV9 (adeno-associated vector type 9) gene transfer of SUMO-1 prevented the heart from hypertrophying following TAC and prevented the development of left ventricular dysfunction. Furthermore, SUMO-1 gene transfer blocked the negative effects of H2O2 on SERCA2a activity in cardiac myocytes, while in vivo indices of oxidative stress were decreased by SUMO-1 in cardiac hypertrophy and heart failure. Conclusion: The results of this study indicate that post-translational modifications of SERCA2a caused by the toxic environment of the hypertrophied and failing myocardium can be prevented by the expression of SUMO-1. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Lippincott Williams & Wilkins Ltd. | - |
dc.title | The Role of/SUMO-1 in Cardiac Oxidative Stress and Hypertrophy | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1161/circ.128.suppl_22.A1842 | - |
dc.identifier.wosid | 000332162907367 | - |
dc.identifier.bibliographicCitation | Circulation, v.128, no.22 | - |
dc.citation.title | Circulation | - |
dc.citation.volume | 128 | - |
dc.citation.number | 22 | - |
dc.type.docType | Meeting Abstract | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.relation.journalResearchArea | Cardiovascular System & Cardiology | - |
dc.relation.journalWebOfScienceCategory | Cardiac & Cardiovascular Systems | - |
dc.relation.journalWebOfScienceCategory | Peripheral Vascular Disease | - |
dc.subject.keywordAuthor | Heart failure | - |
dc.subject.keywordAuthor | Hypertrophy | - |
dc.subject.keywordAuthor | Gene therapy | - |
dc.subject.keywordAuthor | Oxidative stress | - |
dc.identifier.url | https://www.ahajournals.org/doi/10.1161/circ.128.suppl_22.A18426 | - |
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