心脏循环血中miRNA-208a在心肌梗死早期的释放
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Release kinetics of circulating miRNA-208a in the early phase of myocardial infarction
背景与目的
心肌肌钙蛋白(cTnI或cTnT)的测定在生化上可以检测心肌梗死。最近的科学研究表明microRNAs(miRNAs)可能成为组织损伤的新生物标志物。
方 法
为了评估心脏循环血中特异性miRNA-208a的释放动力学,并检验miRNA-208a作为ST段抬高型急性心肌梗死(STEMI)血浆敏感性标志物假说的可行性。研究了19名STEMI患者(4名女性和15名男性,年龄44-85岁),12名稳定型冠心病(CAD)患者和8名CAD阴性患者作为对照组。在入院时以及之后的3,6,12,24和48小时采集血样;在CAD和对照组中,血液样本仅取一次。通过实时聚合酶链反应计算测定的miRNA-208a的血浆水平及其相对倍数变化。在患者的血清样品中也测量cTnI和肌酸激酶(CK)-MB。
结 果
在入院时,STEMI患者血浆中的miRNA-208a增加,在CAD患者和对照组中几乎检测不到其增加。在再灌注后3小时观察到miRNA-208a的峰值(p <0.001)。观察到传统的生物标志物(cTnI和CK-MBmass)与miRNA-208a比较后有明显增加,并在再灌注后6小时达到最大浓度。血浆中miRNA-208a水平与从梗死区域释放的cTnI和CK-MB有很大相关性。
结 论
血浆miRNA-208a有望成为心肌梗死发作后早期释放的新生物标志物之一。
原始文献摘要
Białek S, Górko D, Zajkowska A, et al. Release kinetics of circulating miRNA-208a, in the early phase of myocardial infarction.[J]. Kardiologia Polska, 2015, 73(8):419-425.
Background: The biochemical confirmation of myocardial infarction is based on cardiac troponin (cTnI or cTnT) determination. Recent scientific results suggested that microRNAs (miRNAs) might become a new biomarker of tissue injury.
Aim: To evaluate the release kinetics of circulating heart-specific miRNA-208a and also to test the hypothesis that miRNA-208a can serve as an accessible, diagnostically sensitive plasma biomarker of ST-elevation acute myocardial infarction (STEMI).
Methods: Nineteen STEMI patients (four women and 15 men, aged 44–85 years), 12 patients with stable coronary artery disease (CAD), and eight patients with a negative observation of CAD as a control group were studied. Blood samples were collected on admission and at three, six, 12, 24, and 48 h afterwards; in the CAD and control group blood samples were taken
only once. Plasma levels of miRNA-208a determined by real-time polymerase chain reaction and their relative fold changes were calculated. cTnI and creatinine kinase (CK)-MB mass were also measured in the patients’ serum samples.
Results: miRNA-208a was increased in STEMI patients at the time of admission and nearly undetectable in CAD patients and controls. The peak of miRNA-208a was observed at 3 h after reperfusion (p < 0.001). The traditional biomarkers (cTnI and CK-MBmass), which increase later in comparison to miRNA-208a reaching the maximum concentrations 6 h after reperfusion,
were observed. Circulating miRNA-208a levels strongly correlated with cTnI and CK-MBmass released from the infarcted area.
Conclusions: These results demonstrate that plasma miRNA-208a is an interesting and promising candidate for a new biomarker released early after onset of myocardial infarction.
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