Myocardial Ischemic Preconditioning Preserves Postischemic Function of the 26S Proteasome Through Diminished Oxidative Damage to 19S Regulatory Particle Subunits

RATIONALE:The ubiquitin proteasome system (UPS) becomes dysfunctional as a result of ischemia/reperfusion (I/R), which may lead to dysregulation of signaling pathways. Ischemic preconditioning (IPC) may prevent dysregulation by preventing UPS dysfunction through inhibition of oxidative damage. OBJEC...

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Bibliographic Details
Published in:Circulation research 2010-06, Vol.106 (12), p.1829-1838
Main Authors: Divald, Andras, Kivity, Shaye, Wang, Ping, Hochhauser, Edith, Roberts, Beth, Teichberg, Saul, Gomes, Aldrin V, Powell, Saul R
Format: Article
Language:English
Subjects:
Animals
bcl-2-Associated X Protein - physiology
Biological and medical sciences
Coronary Occlusion - physiopathology
Fundamental and applied biological sciences. Psychology
Heart - physiopathology
Ischemic Preconditioning, Myocardial
Male
Mice
Mice, Inbred Strains
Models, Animal
Myocardial Ischemia - physiopathology
Oxidative Stress - physiology
Proteasome Endopeptidase Complex - physiology
Rats
Rats, Sprague-Dawley
Ubiquitin - physiology
Vertebrates: cardiovascular system
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Summary:RATIONALE:The ubiquitin proteasome system (UPS) becomes dysfunctional as a result of ischemia/reperfusion (I/R), which may lead to dysregulation of signaling pathways. Ischemic preconditioning (IPC) may prevent dysregulation by preventing UPS dysfunction through inhibition of oxidative damage. OBJECTIVE:Examine the hypothesis that early IPC preserves postischemic UPS function thus facilitating prosurvival signaling events. METHODS AND RESULTS:I/R decreased proteasome chymotryptic activity by 50% in isolated rat heart and an in vivo murine left anterior descending coronary artery occlusion model. Following IPC, proteasome activity was decreased 25% (P
ISSN:0009-7330
1524-4571
DOI:10.1161/CIRCRESAHA.110.219485