MiR-543 Regulates the Development of Chronic Obstructive Pulmonary Disease by Targeting Interleukin-33.

BACKGROUND: This main aim of the study was to evaluate the expression and specific role of miR-543 in the progression of chronic obstructive pulmonary disease (COPD), thereby evaluating their diagnostic ability and treatment in COPD patients. METHODS: Real time PCR was carried out to explore the level of miR-543 in the plasma and lung tissues of COPD patients and controls. ELISA was performed to analyze the level of interleukin-33 (IL-33). Dual luciferase was used to validate the target gene of miR-543. RESULTS: First, we showed that the level of miR-543 was increased in the plasma and lung tissues of COPD patients than those of healthy control. Receiver operating characteristic (ROC) analysis indicated that plasma miR-543 could differentiate COPD patients from healthy controls. More importantly, we found that plasma miR-543 was gradually decreased in COPD patients according to FEV1 ≤ 80% (mild), 50% ≤ FEV1 < 80% (moderate), 30% ≤ FEV1 < 50% (moderate), FEV1 < 30% (very severe). Meanwhile, miR-543 was also decreased in COPD patients according to 6MWD ≥ 350 m (mild), 250 m ≤ 6MWD < 349 m (moderate), 150 m ≤ 6MWD < 249 m (severe), and 6MWD ≤ 149 m (very severe). Dual luciferase reporter assay showed that IL-33 was a target gene of miR-543. CONCLUSIONS: In summary, we showed novel data that decreased plasma miR-543 may enhance the progression of COPD via targeting IL-33. Furthermore, plasma miR-543 could be used as a potential non-invasive biomarker for COPD patients, which may shed light on the diagnosis and therapy of COPD.

Plasma miR-18 Screens Acute Myocardial Infarction from Healthy Controls by Targeting Hypoxia Inducible Factor 1α.

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.