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Soluble receptor for advanced glycation end-products protects against ischemia/reperfusion-induced myocardial apoptosis via regulating the ubiquitin proteasome system

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机构: [1]Capital Med Univ,Beijing Tian Tan Hosp,Dept Cardiol,6 Tiantan Xili,Beijing 100050,Peoples R China [2]Capital Med Univ, Dept Physiol & Pathophysiol, Beijing 100069, Peoples R China [3]Dalian Med Univ, Inst Cardiovasc Dis, Affiliated Hosp 1, Dalian 116011, Peoples R China [4]Capital Med Univ, Beijing Tian Tan Hosp, Dept Cardiol, Dept Geriatr, Beijing 100050, Peoples R China
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关键词: ISCHEMIA-REPERFUSION INJURY INDUCED CARDIOPROTECTION PSMB5 PROTEIN MURINE MODEL CELL-DEATH EXPRESSION HEART CARDIOMYOCYTES PATHWAY RAGE

摘要:
Aim: Apoptosis participated in the pathological process of myocardial ischemia/reperfusion (I/R) injury. Previous studies have reported that endogenous substance sRAGE protect against I/R injury through inhibiting myocardial apoptosis. But the mechanisms are currently unknown. Prior work has demonstrated that ubiquitin proteasome system (UPS) dysfunction is closely related to apoptosis. We explored the potential role of UPS in the effect of sRAGE inhibition on I/R-induced myocardial apoptosis. Methods and results: Adult male C57BL mice treated with sRAGE (100 mu g/day, i.p.) or saline were performed to ligate left anterior descending coronary artery (LAD) as an in vivo model. As an in vitro model, primary murine cardiomyocytes pretreated with sRAGE or sRAGE-containing adenovirus were simulated I/R by "ischemia buffer". The TUNEL and caspase-3 activity were assessed. Also the activity and expression of proteasome were detected. sRAGE decreased the number of TUNEL-positive cardiomyocytes and caspase-3 activity, however, the inhibition of sRAGE on I/R-induced apoptosis was abolished by proteasome inhibitor Bortezimb (BTZ). sRAGE inhibited the decreased proteasome activity, also the reduction in protein and gene levels of beta 1i and beta 5i following I/R. Suppression of STAT3 blocked the inhibition of sRAGE on apoptosis induced by I/R. The chromatin immunoprecipitation (CHIP) results confirmed that sRAGE promoted activating STAT3 binding to beta 1i and beta 5i promoter. Conclusions: Our data suggest that the inhibition of sRAGE on I/R-induced apoptosis is associated with activation and expression of proteasome, including improved proteasome activity and elevated beta 1i and beta 5i expression mediated by STAT3 activation. We predict that sRAGE is a novel intervention to target UPS activation for preventing and treating myocardial apoptosis. (C) 2016 Elsevier Inc. All rights reserved.

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基金编号: 2013-3-046 30801217 20108050 81570321 81370313

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出版当年[2015]版:
大类 | 2 区 医学
小类 | 2 区 生化与分子生物学 2 区 内分泌学与代谢
最新[2023]版:
大类 | 2 区 生物学
小类 | 2 区 生化与分子生物学 2 区 内分泌学与代谢
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第一作者机构: [1]Capital Med Univ,Beijing Tian Tan Hosp,Dept Cardiol,6 Tiantan Xili,Beijing 100050,Peoples R China [*1]Capital Med Univ,Beijing Tian Tan Hosp,Dept Cardiol,6 Tiantan Xili,Beijing 100050,Peoples R China
通讯作者:
通讯机构: [1]Capital Med Univ,Beijing Tian Tan Hosp,Dept Cardiol,6 Tiantan Xili,Beijing 100050,Peoples R China [*1]Capital Med Univ,Beijing Tian Tan Hosp,Dept Cardiol,6 Tiantan Xili,Beijing 100050,Peoples R China
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