Myocardial Ischemic Preconditioning Preserves Postischemic Function of the 26S Proteasome Through Diminished Oxidative Damage to 19S Regulatory Particle Subunits
Myocardial Ischemic Preconditioning Preserves Postischemic Function of the 26S Proteasome Through Diminished Oxidative Damage to 19S Regulatory Particle Subunits
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DOI：
10.1161/circresaha.110.219485
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发表时间：
2010-06-25
影响因子：
20.1
通讯作者：
Powell, Saul R.
中科院分区：
文献类型：
--
作者：
Divald, Andras;Kivity, Shaye;Powell, Saul R.
原理：泛素蛋白酶体系统（UPS）由于缺血/再灌注（I/R）而功能失调，这可能导致信号通路失调。缺血预处理（IPC）可能通过抑制氧化损伤来防止UPS功能障碍，从而预防失调。目的：验证早期IPC是否保留了缺血后UPS功能，从而促进了促生存信号事件的发生。方法与结果：I/R可使离体大鼠心脏和活体小鼠左冠状动脉前降支闭塞模型中蛋白酶体的凝乳胰酶活性降低50%。IPC后，蛋白酶体活性降低25% (P
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