Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction
DC Field | Value | Language |
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dc.contributor.author | Xu, Xin | - |
dc.contributor.author | Zhang, Ping | - |
dc.contributor.author | Kwak, Dong min | - |
dc.contributor.author | Fassett, John | - |
dc.contributor.author | Yue, Wenhui | - |
dc.contributor.author | Atzler, Dorothee | - |
dc.contributor.author | Hu, Xinli | - |
dc.contributor.author | Liu, Xiaohong | - |
dc.contributor.author | Wang, Huan | - |
dc.contributor.author | Lu, Zhongbing | - |
dc.contributor.author | Guo, Haipeng | - |
dc.contributor.author | Schwedhelm, Edzard | - |
dc.contributor.author | Böger, Rainer H. | - |
dc.contributor.author | Chen, Peijie | - |
dc.contributor.author | Chen, Yingjie | - |
dc.date.accessioned | 2021-06-22T15:22:41Z | - |
dc.date.available | 2021-06-22T15:22:41Z | - |
dc.date.created | 2021-01-22 | - |
dc.date.issued | 2017-09 | - |
dc.identifier.issn | 0300-8428 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/11590 | - |
dc.description.abstract | Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability. Dimethylarginine dimethylaminohydrolase-1 (DDAH1) exerts a critical role for ADMA degradation and plays an important role in NO signaling. In the heart, DDAH1 is observed in endothelial cells and in the sarcolemma of cardiomyocytes. While NO signaling is important for cardiac adaptation to stress, DDAH1 impact on cardiomyocyte homeostasis is not clear. Here we used the MerCreMer-LoxP model to specifically disrupt cardiomyocyte DDAH1 expression in adult mice to determine the physiological impact of cardiomyocyte DDAH1 under basal conditions and during hypertrophic stress imposed by transverse aortic constriction (TAC). Under control conditions, cardiomyocyte-specific DDAH1 knockout (cDDAH KO) had no detectable effect on plasma ADMA and left ventricular (LV) hypertrophy or function in adult or aging mice. In response to TAC, DDAH1 levels were elevated 2.5-fold in WT mice, which exhibited no change in LV or plasma ADMA content and moderate LV hypertrophy and LV dysfunction. In contrast, cDDAH1 KO mice exposed to TAC showed no increase in LV DDAH1 expression, slightly increased LV tissue ADMA levels, no increase in plasma ADMA, but significantly exacerbated LV hypertrophy, fibrosis, nitrotyrosine production, and LV dysfunction. These findings indicate cardiomyocyte DDAH1 activity is dispensable for cardiac function under basal conditions, but plays an important role in attenuating cardiac hypertrophy and ventricular remodeling under stress conditions, possibly through locally confined regulation of subcellular ADMA and NO signaling. © 2017, Springer-Verlag GmbH Germany. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | Dr. Dietrich Steinkopff Verlag GmbH and Co. KG | - |
dc.title | Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kwak, Dong min | - |
dc.identifier.doi | 10.1007/s00395-017-0644-z | - |
dc.identifier.scopusid | 2-s2.0-85027722643 | - |
dc.identifier.bibliographicCitation | Basic Research in Cardiology, v.112, no.5, pp.1 - 11 | - |
dc.relation.isPartOf | Basic Research in Cardiology | - |
dc.citation.title | Basic Research in Cardiology | - |
dc.citation.volume | 112 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 11 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cardiovascular System & Cardiology | - |
dc.relation.journalWebOfScienceCategory | Cardiac & Cardiovascular Systems | - |
dc.subject.keywordPlus | dimethylargininase | - |
dc.subject.keywordPlus | dimethylarginine dimethylaminohydrolase 1 | - |
dc.subject.keywordPlus | unclassified drug | - |
dc.subject.keywordPlus | 3-nitrotyrosine | - |
dc.subject.keywordPlus | 6 n,n&apos | - |
dc.subject.keywordPlus | dimethylarginine | - |
dc.subject.keywordPlus | amidase | - |
dc.subject.keywordPlus | arginine | - |
dc.subject.keywordPlus | atrial natriuretic factor | - |
dc.subject.keywordPlus | dimethylargininase | - |
dc.subject.keywordPlus | N,N-dimethylarginine | - |
dc.subject.keywordPlus | nitric oxide | - |
dc.subject.keywordPlus | tyrosine | - |
dc.subject.keywordPlus | adult | - |
dc.subject.keywordPlus | animal experiment | - |
dc.subject.keywordPlus | animal tissue | - |
dc.subject.keywordPlus | Article | - |
dc.subject.keywordPlus | cardiac muscle cell | - |
dc.subject.keywordPlus | controlled study | - |
dc.subject.keywordPlus | heart hemodynamics | - |
dc.subject.keywordPlus | heart left ventricle ejection fraction | - |
dc.subject.keywordPlus | heart ventricle failure | - |
dc.subject.keywordPlus | heart ventricle hypertrophy | - |
dc.subject.keywordPlus | homeostasis | - |
dc.subject.keywordPlus | immunoprecipitation | - |
dc.subject.keywordPlus | mouse | - |
dc.subject.keywordPlus | nonhuman | - |
dc.subject.keywordPlus | protein analysis | - |
dc.subject.keywordPlus | protein expression | - |
dc.subject.keywordPlus | protein function | - |
dc.subject.keywordPlus | protein interaction | - |
dc.subject.keywordPlus | signal transduction | - |
dc.subject.keywordPlus | analogs and derivatives | - |
dc.subject.keywordPlus | animal | - |
dc.subject.keywordPlus | blood | - |
dc.subject.keywordPlus | deficiency | - |
dc.subject.keywordPlus | disease model | - |
dc.subject.keywordPlus | enzymology | - |
dc.subject.keywordPlus | fibrosis | - |
dc.subject.keywordPlus | genetic predisposition | - |
dc.subject.keywordPlus | genetics | - |
dc.subject.keywordPlus | heart left ventricle function | - |
dc.subject.keywordPlus | heart left ventricle hypertrophy | - |
dc.subject.keywordPlus | heart ventricle remodeling | - |
dc.subject.keywordPlus | knockout mouse | - |
dc.subject.keywordPlus | male | - |
dc.subject.keywordPlus | metabolism | - |
dc.subject.keywordPlus | pathology | - |
dc.subject.keywordPlus | pathophysiology | - |
dc.subject.keywordPlus | phenotype | - |
dc.subject.keywordPlus | prevention and control | - |
dc.subject.keywordPlus | Amidohydrolases | - |
dc.subject.keywordPlus | Animals | - |
dc.subject.keywordPlus | Arginine | - |
dc.subject.keywordPlus | Atrial Natriuretic Factor | - |
dc.subject.keywordPlus | Disease Models, Animal | - |
dc.subject.keywordPlus | Fibrosis | - |
dc.subject.keywordPlus | Genetic Predisposition to Disease | - |
dc.subject.keywordPlus | Hypertrophy, Left Ventricular | - |
dc.subject.keywordPlus | Male | - |
dc.subject.keywordPlus | Mice, Knockout | - |
dc.subject.keywordPlus | Myocytes, Cardiac | - |
dc.subject.keywordPlus | Nitric Oxide | - |
dc.subject.keywordPlus | Phenotype | - |
dc.subject.keywordPlus | Signal Transduction | - |
dc.subject.keywordPlus | Tyrosine | - |
dc.subject.keywordPlus | Ventricular Dysfunction, Left | - |
dc.subject.keywordPlus | Ventricular Function, Left | - |
dc.subject.keywordPlus | Ventricular Remodeling | - |
dc.subject.keywordAuthor | ADMA | - |
dc.subject.keywordAuthor | Nitric oxide | - |
dc.subject.keywordAuthor | Ventricular hypertrophy | - |
dc.identifier.url | https://www.scopus.com/record/display.uri?eid=2-s2.0-85027722643&origin=inward&txGid=42e41501ec9cdee766173832d8e20294 | - |
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