血管紧张素-（1-7）Mas受体激动剂（AVE 0991）对载脂蛋白E基因敲除小鼠肾脏线粒体蛋白质组的影响
The influence of angiotensin-(1-7) Mas receptor agonist (AVE 0991) on mitochondrial proteome in kidneys of apoE knockout mice.
作者信息
Suski Maciej, Olszanecki Rafał, Stachowicz Aneta, Madej Józef, Bujak-Giżycka Beata, Okoń Krzysztof, Korbut Ryszard
机构信息
Chair of Pharmacology, Jagiellonian University Medical College, 16 Grzegorzecka Str, 31 531, Krakow, Poland.
出版信息
Biochim Biophys Acta. 2013 Dec;1834(12):2463-9. doi: 10.1016/j.bbapap.2013.08.008. Epub 2013 Aug 27.
Excessive action of angiotensin II on mitochondria has been shown to play an important role in mitochondrial dysfunction, a common feature of atherogenesis and kidney injury. Angiotensin-(1-7)/Mas receptor axis constitutes a countermeasure to the detrimental effects of angiotensin II on AT1 receptors. The aim of the study was to assess the effects of angiotensin-(1-7) peptidomimetic AVE0991 on the kidney mitochondrial proteome in widely used animal model of atherosclerosis (apoE(-/-) mice). Proteins changed in apoE(-/-) mice belonged to the groups of antioxidant enzymes, apoptosis regulators, inflammatory factors and metabolic enzymes. Importantly, AVE0991 partially reversed atherosclerosis-related changes in apoE(-/-) mice.
血管紧张素II对线粒体的过度作用已被证明在线粒体功能障碍中起重要作用，而线粒体功能障碍是动脉粥样硬化和肾损伤的一个共同特征。血管紧张素-（1-7）/Mas受体轴是对抗血管紧张素II对AT1受体有害作用的一种应对机制。本研究的目的是评估血管紧张素-（1-7）拟肽AVE0991对广泛使用的动脉粥样硬化动物模型（载脂蛋白E基因敲除小鼠）肾脏线粒体蛋白质组的影响。载脂蛋白E基因敲除小鼠中发生变化的蛋白质属于抗氧化酶、凋亡调节因子、炎症因子和代谢酶组。重要的是，AVE0991部分逆转了载脂蛋白E基因敲除小鼠中与动脉粥样硬化相关的变化。
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