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首页> 外文期刊>Journal of Cellular Physiology >Alteration in Phospholipidome Profile of Myoblast H9c2 Cell Line in a Model of Myocardium Starvation and Ischemia
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Alteration in Phospholipidome Profile of Myoblast H9c2 Cell Line in a Model of Myocardium Starvation and Ischemia

机译：变更成肌细胞的Phospholipidome概要文件H9c2细胞系模型的心肌饥饿和缺血

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摘要

Myocardium infarction is one of the most deathly cardiovascular diseases. It is characterized by myocardium ischemia as a result of nutrients depletion and hypoxia. The cell can respond to this injury by autophagy or apoptosis, which determines the evolution and possible recovery of the myocardium infarction. Lipids play an important role in cardiovascular disease. However reports stating lipidome variations in cardiovascular disease are scarce and the role that lipids play in this pathological condition is not completely understood. The aim of this work was to identify changes in lipid profile of a myoblast H9c2 cell line under starvation and ischemia, to better understand and recognize new biomarkers for myocardial infarction. Lipidomic profile was evaluated by HILIC-LC-MS and GC-MS. Cardiac cells showed alterations in phosphatidylcholines PC (34:1) and PC (36:2), lysophosphatidylcholines lyso PC(16:0), lysoPC(18:1) and lysoPC(18:0), phosphatidylethanolamine PE (34:1), phosphatidylserine PS (36:1), phosphatidylinositol PI (36:2), PI (38:3) and PI (38:5), sphingomyelin SM (34:1) and cardiolipins CL(68:4), CL(72:5) and CL(74:7) in ischemia and/or starvation, in comparison with control. Specific differences observed only in starvation were decrease of SM (34:1) and FA (20:4), and increase of PS (36:1). Differences observed only in ischemia were decrease of PC (36:2), lyso PC (16:0) and FA (18:1) and simultaneous increase of FA (16:0), and FA (18:0). Interestingly, PC (34:1) increased in ischemia and decreased in starvation. In conclusion, our work suggests that lipids are potential markers for evaluation of cell fate, either cell death or recovery, which will be useful to improve diagnosis and prognostic of cardiovascular diseases. J. Cell. Physiol. 231: 2266-2274, 2016. (c) 2016 Wiley Periodicals, Inc.
机译：心肌梗死是一种最致命的心血管疾病。心肌缺血的营养素损耗和缺氧。自噬和凋亡伤,决定了进化和可能的恢复心肌梗死。在心血管疾病的重要作用。报告称lipidome变化心血管疾病是稀缺和角色脂质在这个病理条件不是完全理解。工作是确定血脂的变化饥饿和下一个成肌细胞H9c2细胞系缺血,更好地理解和认识新生物标记心肌梗死。配置文件由HILIC-LC-MS评估,gc - ms。心肌细胞显示改变磷脂酰胆碱PC(34:1)和PC (36:2),lysophosphatidylcholines lyso PC (16:0),磷脂酰丝氨酸PS (36:1),CL (68:4), CL(72:5)和CL(74:7)缺血和/或饥饿,相比,控制。观察到的特定差异只有在饥饿减少了SM(34:1)和FA(20:4),然后呢增加了PS(36:1)。在缺血减少电脑(36:2)lyso电脑(16:0)和FA(第18章)和同步增长FA(16:0)和FA(18:0)。(34:1)增加缺血和减少饥饿。脂类是评估潜在的标记细胞命运,细胞死亡或恢复将有助于改善诊断和心血管疾病的预后。杂志。231:2266 - 2274年,2016年。期刊、公司。

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