SUMO1-dependent modulation of SERCA2a in heart failure

Changwon Kho, Ahyoung Lee, Dongtak Jeong, Jae Gyun Oh, Antoine H. Chaanine, Eddy Kizana, Woo Jin Park and Roger J. Hajjar ()
Additional contact information
Changwon Kho: Cardiovascular Research Center, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1030
Ahyoung Lee: Cardiovascular Research Center, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1030
Dongtak Jeong: Cardiovascular Research Center, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1030
Jae Gyun Oh: College of Life Sciences, Gwangju Institute of Science and Technology, 261 Cheomdan-gwagiro, Buk-gu
Antoine H. Chaanine: Cardiovascular Research Center, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1030
Eddy Kizana: Westmead Millennium Institute, Westmead Hospital
Woo Jin Park: College of Life Sciences, Gwangju Institute of Science and Technology, 261 Cheomdan-gwagiro, Buk-gu
Roger J. Hajjar: Cardiovascular Research Center, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1030

Nature, 2011, vol. 477, issue 7366, 601-605

Abstract: SUMO1 level linked to heart failure SERCA2a is an ATPase responsible for calcium reuptake during excitation contraction coupling. Levels and activity of SERCA2a are decreased in heart failure, and a gene-therapy approach to deliver SERCA2a to failing hearts is being tested in clinical trials. Roger Hajjar and colleagues now show that SUMOylation, the attachment of SUMO (small ubiquitin-like modifier) proteins, is essential for preserving the stability and activity of SERCA2a and that levels of SUMO1 are decreased in failing hearts. They also show in a mouse model of heart failure that gene delivery of SUMO1 can restore heart function to the same degree as delivery of SERCA2a, pointing to SUMO1 as a potential therapeutic candidate for treating heart failure.

Date: 2011
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DOI: 10.1038/nature10407

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