Adenosine kinase attenuates cardiomyocyte microtubule stabilization and protects against pressure overload-induced hypertrophy and LV dysfunction
DC Field | Value | Language |
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dc.contributor.author | Fassett, John | - |
dc.contributor.author | Xu, Xin | - |
dc.contributor.author | Kwak, Dongmin | - |
dc.contributor.author | Zhu, Guangshuo | - |
dc.contributor.author | Fassett, Erin K. | - |
dc.contributor.author | Zhang, Ping | - |
dc.contributor.author | Wang, Huan | - |
dc.contributor.author | Mayer, Bernd | - |
dc.contributor.author | Bache, Robert J. | - |
dc.contributor.author | Chen, Yingjie | - |
dc.date.accessioned | 2021-06-22T10:41:11Z | - |
dc.date.available | 2021-06-22T10:41:11Z | - |
dc.date.created | 2021-05-13 | - |
dc.date.issued | 2019-05 | - |
dc.identifier.issn | 0022-2828 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/3938 | - |
dc.description.abstract | Adenosine exerts numerous protective actions in the heart, including attenuation of cardiac hypertrophy. Adenosine kinase (ADK) converts adenosine to adenosine monophosphate (AMP) and is the major route of myocardial adenosine metabolism, however, the impact of ADK activity on cardiac structure and function is unknown. To examine the role of ADK in cardiac homeostasis and adaptation to stress, conditional cardiomyocyte specific ADK knockout mice (cADK −/− ) were produced using the MerCreMer-lox-P system. Within 4 weeks of ADK disruption, cADK −/− mice developed spontaneous hypertrophy and increased β-Myosin Heavy Chain expression without observable LV dysfunction. In response to 6 weeks moderate left ventricular pressure overload (transverse aortic constriction;TAC), wild type mice (WT) exhibited ~60% increase in ventricular ADK expression and developed LV hypertrophy with preserved LV function. In contrast, cADK −/− mice exhibited significantly greater LV hypertrophy and cardiac stress marker expression (atrial natrurietic peptide and β-Myosin Heavy Chain), LV dilation, reduced LV ejection fraction and increased pulmonary congestion. ADK disruption did not decrease protein methylation, inhibit AMPK, or worsen fibrosis, but was associated with persistently elevated mTORC1 and p44/42 ERK MAP kinase signaling and a striking increase in microtubule (MT) stabilization/detyrosination. In neonatal cardiomyocytes exposed to hypertrophic stress, 2-chloroadenosine (CADO) or adenosine treatment suppressed MT detyrosination, which was reversed by ADK inhibition with iodotubercidin or ABT-702. Conversely, adenoviral over-expression of ADK augmented CADO destabilization of MTs and potentiated CADO attenuation of cardiomyocyte hypertrophy. Together, these findings indicate a novel adenosine receptor-independent role for ADK-mediated adenosine metabolism in cardiomyocyte microtubule dynamics and protection against maladaptive hypertrophy. © 2019 | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | Academic Press | - |
dc.title | Adenosine kinase attenuates cardiomyocyte microtubule stabilization and protects against pressure overload-induced hypertrophy and LV dysfunction | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kwak, Dongmin | - |
dc.identifier.doi | 10.1016/j.yjmcc.2019.03.015 | - |
dc.identifier.scopusid | 2-s2.0-85063376664 | - |
dc.identifier.wosid | 000468257200005 | - |
dc.identifier.bibliographicCitation | Journal of Molecular and Cellular Cardiology, v.130, pp.49 - 58 | - |
dc.relation.isPartOf | Journal of Molecular and Cellular Cardiology | - |
dc.citation.title | Journal of Molecular and Cellular Cardiology | - |
dc.citation.volume | 130 | - |
dc.citation.startPage | 49 | - |
dc.citation.endPage | 58 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cardiovascular System & CardiologyCell Biology | - |
dc.relation.journalWebOfScienceCategory | Cardiac & Cardiovascular SystemsCell Biology | - |
dc.subject.keywordPlus | 2 chloroadenosine | - |
dc.subject.keywordPlus | adenosine kinase | - |
dc.subject.keywordPlus | adenosine phosphate | - |
dc.subject.keywordPlus | atrial natriuretic factor | - |
dc.subject.keywordPlus | mammalian target of rapamycin complex 1 | - |
dc.subject.keywordPlus | mitogen activated protein kinase | - |
dc.subject.keywordPlus | myosin heavy chain beta | - |
dc.subject.keywordPlus | adenosine kinase | - |
dc.subject.keywordPlus | hydroxymethylglutaryl coenzyme A reductase kinase | - |
dc.subject.keywordPlus | adaptation | - |
dc.subject.keywordPlus | animal cell | - |
dc.subject.keywordPlus | aortic constriction | - |
dc.subject.keywordPlus | Article | - |
dc.subject.keywordPlus | attenuation | - |
dc.subject.keywordPlus | cardiac muscle cell | - |
dc.subject.keywordPlus | cell disruption | - |
dc.subject.keywordPlus | controlled study | - |
dc.subject.keywordPlus | detyrosination | - |
dc.subject.keywordPlus | disease exacerbation | - |
dc.subject.keywordPlus | disease marker | - |
dc.subject.keywordPlus | enzyme activity | - |
dc.subject.keywordPlus | enzyme regulation | - |
dc.subject.keywordPlus | fibrosis | - |
dc.subject.keywordPlus | heart function | - |
dc.subject.keywordPlus | heart left ventricle ejection fraction | - |
dc.subject.keywordPlus | heart left ventricle failure | - |
dc.subject.keywordPlus | heart left ventricle function | - |
dc.subject.keywordPlus | heart left ventricle hypertrophy | - |
dc.subject.keywordPlus | heart left ventricle overload | - |
dc.subject.keywordPlus | heart muscle metabolism | - |
dc.subject.keywordPlus | heart protection | - |
dc.subject.keywordPlus | heart stress | - |
dc.subject.keywordPlus | heart ventricle hypertrophy | - |
dc.subject.keywordPlus | homeostasis | - |
dc.subject.keywordPlus | immunohistochemistry | - |
dc.subject.keywordPlus | in vivo study | - |
dc.subject.keywordPlus | knockout mouse | - |
dc.subject.keywordPlus | lung congestion | - |
dc.subject.keywordPlus | male | - |
dc.subject.keywordPlus | membrane stabilization | - |
dc.subject.keywordPlus | microtubule | - |
dc.subject.keywordPlus | mouse | - |
dc.subject.keywordPlus | newborn | - |
dc.subject.keywordPlus | nonhuman | - |
dc.subject.keywordPlus | nucleic acid metabolism | - |
dc.subject.keywordPlus | priority journal | - |
dc.subject.keywordPlus | protein expression | - |
dc.subject.keywordPlus | protein methylation | - |
dc.subject.keywordPlus | protein modification | - |
dc.subject.keywordPlus | protein stability | - |
dc.subject.keywordPlus | rat | - |
dc.subject.keywordPlus | signal transduction | - |
dc.subject.keywordPlus | stress | - |
dc.subject.keywordPlus | wild type mouse | - |
dc.subject.keywordPlus | animal | - |
dc.subject.keywordPlus | cardiac muscle cell | - |
dc.subject.keywordPlus | cardiomegaly | - |
dc.subject.keywordPlus | genetics | - |
dc.subject.keywordPlus | heart stroke volume | - |
dc.subject.keywordPlus | MAPK signaling | - |
dc.subject.keywordPlus | metabolism | - |
dc.subject.keywordPlus | microtubule | - |
dc.subject.keywordPlus | pathology | - |
dc.subject.keywordPlus | pathophysiology | - |
dc.subject.keywordPlus | Sprague Dawley rat | - |
dc.subject.keywordPlus | Adenosine Kinase | - |
dc.subject.keywordPlus | AMP-Activated Protein Kinases | - |
dc.subject.keywordPlus | Animals | - |
dc.subject.keywordPlus | Cardiomegaly | - |
dc.subject.keywordPlus | MAP Kinase Signaling System | - |
dc.subject.keywordPlus | Mice | - |
dc.subject.keywordPlus | Mice, Knockout | - |
dc.subject.keywordPlus | Microtubules | - |
dc.subject.keywordPlus | Myocytes, Cardiac | - |
dc.subject.keywordPlus | Rats | - |
dc.subject.keywordPlus | Rats, Sprague-Dawley | - |
dc.subject.keywordPlus | Stroke Volume | - |
dc.subject.keywordPlus | Ventricular Dysfunction, Left | - |
dc.subject.keywordAuthor | Adenosine | - |
dc.subject.keywordAuthor | Adenosine kinase | - |
dc.subject.keywordAuthor | Cardiac hypertrophy | - |
dc.subject.keywordAuthor | Detyrosinated tubulin | - |
dc.subject.keywordAuthor | Microtubules | - |
dc.identifier.url | https://www.scopus.com/record/display.uri?eid=2-s2.0-85063376664&origin=inward&txGid=399dc01756a1e5669ed42e1736ee3990 | - |
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