The cellular prion protein counteracts cardiac oxidative stress.
The cellular prion protein counteracts cardiac oxidative stress.
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细胞朊病毒蛋白抵消心脏氧化应激
DOI：
10.1093/cvr/cvu194
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发表时间：
2014
影响因子：
10.8
通讯作者：
Di Lisa F
中科院分区：
文献类型：
--
作者：
Zanetti F;Carpi A;Menabò R;Giorgio M;Schulz R;Valen G;Baysa A;Massimino ML;Sorgato MC;Bertoli A;Di Lisa F
细胞朊蛋白PrPC的异常亚型与人和动物的朊病毒疾病有关，其生理功能尚不清楚。已经观察到增加表达的PrPC在两个体内的心脏重塑的paradigms，我们专注于离体小鼠心脏，以确定能力的PrPC拮抗氧化损伤诱导缺血和非缺血protocols.Methods和resultsHearts从小鼠分离表达PrPC在变量进行不同的和互补的氧化灌注协议。评价活性氧的积累、肌原纤维蛋白的氧化和细胞死亡。我们发现，过表达PrPC减少缺血后再灌注引起的氧化应激和细胞死亡。相反，删除PrPC增加氧化应激在缺血预处理和灌注（15分钟）与H2O2。支持其与细胞内系统参与氧化应激的关系，PrPC被发现影响过氧化氢酶的活性，第一次，p66 Shc的表达，一种蛋白质牵连在氧化应激介导的细胞death.ConclusionsOur数据表明，PrPC有助于心脏机制拮抗氧化损伤。
AimsThe cellular prion protein, PrPC, whose aberrant isoforms are related to prion diseases of humans and animals, has a still obscure physiological function. Having observed an increased expression of PrPCin twoin vivoparadigms of heart remodelling, we focused on isolated mouse hearts to ascertain the capacity of PrPCto antagonize oxidative damage induced by ischaemic and non-ischaemic protocols.Methods and resultsHearts isolated from mice expressing PrPCin variable amounts were subjected to different and complementary oxidative perfusion protocols. Accumulation of reactive oxygen species, oxidation of myofibrillar proteins, and cell death were evaluated. We found that overexpressed PrPCreduced oxidative stress and cell death caused by post-ischaemic reperfusion. Conversely, deletion of PrPCincreased oxidative stress during both ischaemic preconditioning and perfusion (15 min) with H2O2. Supporting its relation with intracellular systems involved in oxidative stress, PrPCwas found to influence the activity of catalase and, for the first time, the expression of p66Shc, a protein implicated in oxidative stress-mediated cell death.ConclusionsOur data demonstrate that PrPCcontributes to the cardiac mechanisms antagonizing oxidative insults.
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影响因子：
6
作者：
C. Peggion;A. Bertoli;M. Sorgato
通讯作者：
C. Peggion;A. Bertoli;M. Sorgato
影响因子：
37.8
作者：
Robert B. Jennings;Charles E. Murry;Charles Steenbergen;K. Reimer
通讯作者：
Robert B. Jennings;Charles E. Murry;Charles Steenbergen;K. Reimer
细胞朊病毒蛋白的过度表达会改变缺血后 Erk1/2 磷酸化，但不会改变 Akt 磷酸化，并可预防局灶性脑缺血。
影响因子：
2.8
作者：
J. Weise;T. Doeppner;T. Müller;A. Wrede;W. Schulz;I. Zerr;O. Witte;M. Bähr
通讯作者：
M. Bähr
影响因子：
7.4
作者：
Oudot, Alexandra;Martin, Caroline;Rochette, Luc
通讯作者：
Rochette, Luc
朊病毒蛋白敲除小鼠
影响因子：
2.3
作者：
Andrew D. Steele;S. Lindquist;A. Aguzzi
通讯作者：
A. Aguzzi