The Role of/SUMO-1 in Cardiac Oxidative Stress and Hypertrophy
- Authors
- Lee, Ahyoung; Jeong, Dongtak; Mitsuyama, Shinichi; Kho, Changwon; Hajjar, Roger J.
- Issue Date
- Nov-2013
- Publisher
- Lippincott Williams & Wilkins Ltd.
- Keywords
- Heart failure; Hypertrophy; Gene therapy; Oxidative stress
- Citation
- Circulation, v.128, no.22
- Indexed
- SCI
SCIE
- Journal Title
- Circulation
- Volume
- 128
- Number
- 22
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/26296
- DOI
- 10.1161/circ.128.suppl_22.A1842
- ISSN
- 0009-7322
1524-4539
- 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.
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