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Author Notes:

Correspondence: John W. Calvert, Ph.D., Department of Surgery, Division of Cardiothoracic Surgery, Carlyle Fraser Heart Center, Emory University School of Medicine, 380 Northyards Boulevard, Suite B, Atlanta, GA 30313, Phone: 404-251-0663, Fax: 404-251-0701, jcalver@emory.edu

Disclosures: none.


Research Funding:

Supported by grants from the National Institutes of Health National Heart Lung and Blood Institute (5R01HL098481-05) to J.W.C. and the American Heart Association (15POST25610016) to Y.S.

This work was also supported by funding from the Carlyle Fraser Heart Center of Emory University Hospital Midtown.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Cardiac & Cardiovascular Systems
  • Cell Biology
  • Cardiovascular System & Cardiology
  • DJ-1
  • Myocardial ischemia
  • Mitochondrial fission
  • SUMOylation
  • SUMO

DJ-1 protects the heart against ischemia-reperfusion injury by regulating mitochondrial fission

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Journal Title:

Journal of Molecular and Cellular Cardiology


Volume 97


, Pages 56-66

Type of Work:

Article | Post-print: After Peer Review


Recent data indicates that DJ-1 plays a role in the cellular response to stress. Here, we aimed to examine the underlying molecular mechanisms mediating the actions of DJ-1 in the heart following myocardial ischemia-reperfusion (I/R) injury. In response to I/R injury, DJ-1 KO mice displayed increased areas of infarction and worsened left ventricular function when compared to WT mice, confirming a protective role for DJ-1 in the heart. In an effort to evaluate the potential mechanism(s) responsible for the increased injury in DJ-1 KO mice, we focused on SUMOylation, a post-translational modification process that regulates various aspects of protein function. DJ-1 KO hearts after I/R injury were found to display enhanced accumulation of SUMO-1 modified proteins and reduced SUMO-2/3 modified proteins. Further analysis, revealed that the protein expression of the de-SUMOylation enzyme SENP1 was reduced, whereas the expression of SENP5 was enhanced in DJ-1 KO hearts after I/R injury. Finally, DJ-1 KO hearts were found to display enhanced SUMO-1 modification of dynamin-related protein 1, excessive mitochondrial fission, and dysfunctional mitochondria. Our data demonstrates that the activation of DJ-1 in response to myocardial I/R injury protects the heart by regulating the SUMOylation status of Drp1 and attenuating excessive mitochondrial fission.

Copyright information:

© 2016 Elsevier Ltd. All rights reserved.

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