BACKGROUND: This study aims to evaluate the expression of plasma miR-18, thereby evaluating its potential use as a biomarker to screen acute myocardial infarction (AMI) patients from healthy controls. METHODS: Real time PCR was carried out to evaluate the level of miR-18 in AMI patients and healthy controls. ROC analysis was performed to evaluate whether miR-18 could be used as a potential biomarker. Dual luciferase assay was used to identify the potential target of miR-18. RESULTS: We showed novel data that plasma miR-18 was significantly greater in AMI patients than in healthy controls. ROC analysis indicated that plasma miR-18 could screen AMI patients from healthy controls with high sensitivity and specificity. Further study demonstrated that plasma miR-18 was positively correlated with serum cardiac troponin I (cTnI) and creatine phosphokinase-MB (CK-MB) concentrations. Additionally, plasma miR-18 was increased in AMI patients with more stenosed coronary vessels. More importantly, plasma miR-18 was decreased in AMI patients after receiving percutaneous coronary intervention (PCI). Dual luciferase reporter assay indicated that overexpression of miR-18 significantly suppressed the relative luciferase activity of pmirGLO- HIF1α-3´UTR. CONCLUSIONS: In summary, enhanced plasma miR-18 could be used as a potential biomarker to screen AMI patients from healthy controls via targeting HIF1α.
BACKGROUND: This study aims to evaluate the expression of plasma miR-18, thereby evaluating its potential use as a biomarker to screen acute myocardial infarction (AMI) patients from healthy controls. METHODS: Real time PCR was carried out to evaluate the level of miR-18 in AMI patients and healthy controls. ROC analysis was performed to evaluate whether miR-18 could be used as a potential biomarker. Dual luciferase assay was used to identify the potential target of miR-18. RESULTS: We showed novel data that plasma miR-18 was significantly greater in AMI patients than in healthy controls. ROC analysis indicated that plasma miR-18 could screen AMI patients from healthy controls with high sensitivity and specificity. Further study demonstrated that plasma miR-18 was positively correlated with serum cardiac troponin I (cTnI) and creatine phosphokinase-MB (CK-MB) concentrations. Additionally, plasma miR-18 was increased in AMI patients with more stenosed coronary vessels. More importantly, plasma miR-18 was decreased in AMI patients after receiving percutaneous coronary intervention (PCI). Dual luciferase reporter assay indicated that overexpression of miR-18 significantly suppressed the relative luciferase activity of pmirGLO- HIF1α-3´UTR. CONCLUSIONS: In summary, enhanced plasma miR-18 could be used as a potential biomarker to screen AMI patients from healthy controls via targeting HIF1α.