The primary objective of this study investigated the role of microRNA-320 (miR-320) on left ventricular remodeling in the rat model of myocardial ischemia-reperfusion (I/R) injury, and we intended to explore the myocardial mechanism of miR-320-mediated myocardium protection. We collected 120 male Wistar rats (240–280 g) in this study and then randomly divided them into three groups: (1) sham surgery group (sham group: n = 40); (2) ischemia-reperfusion model group (I/R group: n = 40); and (3) I/R model with antagomir-320 group (I/R + antagomir-320 group: n = 40). Value changes of heart function in transesophageal echocardiography were recorded at various time points (day 1, day 3, day 7, day 15 and day 30) after surgery in each group. Myocardial sections were stained with hematoxylin and eosin (H&E) and examined with optical microscope. The degree of myocardial fibrosis was assessed by Sirius Red staining. Terminal dUTP nick end-labeling (TUNEL) and qRT-PCR methods were used to measure the apoptosis rate and to determine the miR-320 expression levels in myocardial tissues. Transesophageal echocardiography showed that the values of left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP) and ±dp/dtmax in the I/R group were obviously lower than those in the sham group, while the left ventricular end-diastolic pressure (LVEDP) value was higher than that in the sham group. The values of LVEF, LVFS, LVSP and ±dp/dtmax showed a gradual decrease in the I/R group, while the LVEDP value showed an up tendency along with the extension of reperfusion time. The H&E staining revealed that rat myocardial tissue in the I/R group presented extensive myocardial damage; for the I/R + antagomir-320 group, however, the degree of damage in myocardial cells was obviously better than that of the I/R group. The Sirius Red staining results showed that the degree of myocardial fibrosis in the I/R group was more severe along with the extension of the time of reperfusion. For the I/R + antagomir-320 group, the degree of myocardial fibrosis was less severe than that in the I/R group. Tissues samples in both the sham and I/R + antagomir-320 groups showed a lower apoptosis rate compared to I/R group. The qRT-PCR results indicated that miR-320 expression in the I/R group was significantly higher than that in both the sham and I/R + antagomir-320 groups. The expression level of miR-320 is significantly up-regulated in the rat model of myocardial I/R injury, and it may be implicated in the prevention of myocardial I/R injury-triggered left ventricular remodeling.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: This study aimed to explore the association of long non-coding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) with exacerbation risk, lung function, and inflammatory cytokines in asthma. Methods:A total of 170 patients with asthma in exacerbation, 170 patients with asthma in remission, and 170 healthy controls (HCs) were enrolled, and their plasma samples were collected. The expressions of lncRNA NEAT1 and microRNA-124 (miRNA-124) in plasma were detected by real-time quantitative polymerase chain reaction; inflammatory cytokines in plasma were measured by the Enzyme-linked immunosorbent assay (ELISA); and pulmonary ventilation function was detected by examination of forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC).Results: LncRNA NEAT1 expression was upregulated in asthma patients in exacerbation compared with HCs and asthma patients in remission, and receiver operating characteristic curve exhibited that it was of good value in distinguishing asthma patients in exacerbation from HCs (AUC: 0.869 (0.830-0.908)) and asthma patients in remission (AUC: 0.775 (0.724-0.825)). Furthermore, lncRNA NEAT1 was positively correlated with exacerbation severity, TNF-α, IL-1β, and IL-17, but negatively correlated with IL-10, FEV 1 /FVC and FEV 1 %predicted in asthma patients. Additionally, lncRNA NEAT1 was negatively correlated with miR-124, and miR-124 was negatively associated with exacerbation risk, exacerbation severity, and inflammation, but positively associated with lung function in asthma patients. Conclusion:Circulating lncRNA NEAT1 exhibits potential to be a new biomarker for elevated exacerbation risk and severity of asthma. K E Y W O R D S asthma, exacerbation, lncRNA NEAT1, miR-124 S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Li X, Ye S, Lu Y. Long non-coding RNA NEAT1 overexpression associates with increased exacerbation risk, severity, and inflammation, as well as decreased lung function through the interaction with microRNA-124 in asthma.

To investigate the correlation of miR-125a/b expression with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) patients and inflammatory cytokines.Eighty-seven AECOPD patients, 93 stable chronic obstructive pulmonary disease (COPD) patients and 100 health volunteers (HCs) were recruited. Plasma samples were collected from AECOPD patients at the day 1, day 7, day 14, and day 28 of admission and from stable COPD patients as well as HCs. Total RNA was extracted from plasma, and miR-125a/b relative expressions were determined by quantitative real time-polymerase chain reaction.MiR-125b had a great capacity for distinguishing AECOPD from stable COPD (AUC = 0.926, 95% CI: 0.884–0.967) and HCs (AUC = 0.923, 95% CI: 0.880–0.966), while miR-125a did not. There were associations between miR-125b expression with TNF-α, IL-8, and LTB-4 in AECOPD patients (P = .012, P = .032, and P = .047, respectively), while no correlation of miR-125a with inflammatory cytokines was found. MiR-125b expression gradually decreased at day 7, day 14, and day 28 compared with day 1 (all P < .05) on admission, while no difference in miR-125a was discovered between each visit compared to day 1. Besides, TNF-α, IL-1β, IL-8, and LTB-4 were elevated in AECOPD patients compared with stable COPD patients (all P < .01).MiR-125b, but not miR-125a, was positively associated with inflammatory cytokines and could be a novel biomarker for distincting AECOPD from stable COPD patients and HCs.