Please use this identifier to cite or link to this item: https://doi.org/10.1161/01.CIR.0000086978.95976.41
DC FieldValue
dc.titleA20 is dynamically regulated in the heart and inhibits the hypertrophic response
dc.contributor.authorCook S.A.
dc.contributor.authorNovikov M.S.
dc.contributor.authorAhn Y.
dc.contributor.authorMatsui T.
dc.contributor.authorRosenzweig A.
dc.date.accessioned2018-11-29T07:17:54Z
dc.date.available2018-11-29T07:17:54Z
dc.date.issued2003
dc.identifier.citationCook S.A., Novikov M.S., Ahn Y., Matsui T., Rosenzweig A. (2003). A20 is dynamically regulated in the heart and inhibits the hypertrophic response. Circulation 108 (6) : 664-667. ScholarBank@NUS Repository. https://doi.org/10.1161/01.CIR.0000086978.95976.41
dc.identifier.issn97322
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/149284
dc.description.abstractBackground - Nuclear factor (NF)-kB signaling has been implicated in cardiomyocyte hypertrophy. Here, we determine the cardiac regulation and biological activity of A20, an inhibitor of NF-kB signaling. Methods and Results - Mice were subjected to aortic banding, and A20 expression was examined. A20 mRNA upregulation (4.3�1.5-fold; P<0.05) was detected 3 hours after banding, coinciding with peak NF-kB activation. A20 was also upregulated in cultured neonatal cardiomyocytes stimulated with phenylephrine or endothelin-1 (2.8�0.6- and 4�1.1-fold, respectively; P<0.05), again paralleling NF-kB activation. Infection of cardiomyocytes with an adenoviral vector (Ad) encoding A20 inhibited tumor necrosis factor-?-stimulated NF-kB signaling with an efficacy comparable to dominant negative inhibitor of k-B kinase ? (dnIKK?). Ad.dnIKK?-infected cardiomyocytes exhibited increased apoptosis when they were serum starved or subjected to hypoxia-reoxygenation, whereas Ad.A20-infected cardiomyocytes did not. Expression of Ad.A20 inhibited the hypertrophic response in cardiomyocytes stimulated with phenylephrine or endothelin-1. Conclusions - A20 is dynamically regulated during acute biomechanical stress in the heart and functions to attenuate cardiac hypertrophy through the inhibition of NF-kB signaling without sensitizing cardiomyocytes to apoptotic cell death.
dc.publisherAHA journals
dc.sourceScopus
dc.subjectApoptosis
dc.subjectHypertrophy
dc.subjectInflammation
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1161/01.CIR.0000086978.95976.41
dc.description.sourcetitleCirculation
dc.description.volume108
dc.description.issue6
dc.description.page664-667
dc.published.statepublished
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