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Expression of the peptide hormone hepcidin increases in cardiomyocytes under myocarditis and myocardial infarction

机译:心肌炎和心肌梗塞下心肌细胞中肽激素hepcidin的表达增加

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The micronutrient iron is an essential component that plays a role in many crucial metabolic reactions. The peptide hormone hepcidin is thought to play a central role in iron homeostasis and its expression is induced by iron overloading and inflammation. Recently, hepcidin has been reported to be expressed also in the heart; however, the kinetics of altered hepcidin expression in diseases of the heart remain unknown. In this study, we examined cardiac expression of hepcidin in rat experimental autoimmune myocarditis (EAM), human myocarditis and rat acute myocardial infarction (AMI). In rat EAM and AMI hearts, hepcidin was expressed in cardiomyocytes; ferroportin, which is a cellular iron exporter bound by hepcidin, was also expressed in various cells. Analysis of the time course of the hepcidin to cytochrome oxidase subunit 6a (Cox6a)2 expression ratio showed that it abruptly increased more than 100-fold in hearts in the very early phase of EAM and in infarcted areas 1 day after MI. The hepcidin/Cox6a2 expression ratio correlated significantly with that of interleukin-6/gamma-actin in both EAM and AMI hearts (r=0.781. P<0001 and r=0.563, P=.0003). In human hearts with histological myocarditis, the ratio was significantly higher than in those without myocarditis (0.0400 +/- 0.0195 versus 0.0032 +/- 0.0017, P=.0045). Hepcidin is strongly induced in cardiomyocytes under myocarditis and MI, conditions in which inflammatory cytokine levels increase and may play an important role in iron homeostasis and free radical generation
机译:微量营养素铁是在许多关键的代谢反应中起作用的重要成分。肽激素铁调素被认为在铁体内平衡中起着核心作用,其表达是由铁超载和炎症诱导的。最近,有报道称铁调素也在心脏中表达。然而,心脏疾病中铁调素表达改变的动力学仍然未知。在这项研究中,我们检查了铁调素在大鼠实验性自身免疫性心肌炎(EAM),人心肌炎和大鼠急性心肌梗死(AMI)中的心脏表达。在大鼠EAM和AMI心脏中,hepcidin在心肌细胞中表达。铁转运蛋白是由铁调素结合的细胞铁输出物,也在各种细胞中表达。分析铁调素与细胞色素氧化酶亚基6a(Cox6a)2的表达比例的时间过程表明,它在EAM的早期和心肌梗死后1天在梗塞区域的心脏中突然增加了100倍以上。在EAM和AMI心脏中,hepcidin / Cox6a2的表达率与白细胞介素6 /γ-肌动蛋白的表达率显着相关(r = 0.781。P <0001和r = 0.563,P = .0003)。在患有组织学性心肌炎的人心脏中,该比率显着高于未患有心肌炎的人心脏(0.0400 +/- 0.0195对0.0032 +/- 0.0017,P = .0045)。 Hepcidin在心肌炎和MI下在心肌细胞中被强烈诱导,炎症细胞因子水平升高并且可能在铁稳态和自由基产生中起重要作用

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