Inflammation-Related MicroRNAs Are Associated with Plaque Stability Calculated by IVUS in Coronary Heart Disease Patients.

OBJECTIVES: This study aimed to investigate the association between inflammation-related microRNAs (miR-21, 146a, 155) and the plaque stability in coronary artery disease patients. METHODS: The expression of miR-21, 146a, and 155 was measured by real-time PCR in 310 consecutive patients. The level of hs-CRP, IL-6, and IL-8 was measured by ELISA. The plaque stability of coronary stenotic lesions was evaluated with intravascular ultrasound (IVUS). RESULTS: (1) The levels of hs-CRP, IL-6, and IL-8 were significantly increased in the UAP and AMI groups compared with the CPS group (P < 0.01). (2) The expression of miR-21 and miR-146a in peripheral blood mononuclear cells (PBMCs) and plasma was significantly higher in CAD patients compared with non-CAD patients, whereas the miR-155 expression in PBMCs and plasma was significantly lower in patients with CAD. (3) The miR-21 expression in PBMCs was higher in UAP and AMI groups compared with CPS group. The miR-146a expression in PBMCs was higher in SAP, UAP, and AMI groups than in CPS group. Although the level of miR-155 in PBMCs was lower in SAP, UAP, and AMI groups than in CPS group. The expression patterns of miR-21, miR-146a, and miR-155 in plasma were consistent with those of PBMCs. (4) The expressions of miR-21 and miR-146a in PBMCs and plasma were significantly higher in the vulnerable plaque group than those in stable plaque group. While miR-155 in PBMCs and plasma was significantly lower in vulnerable plaque group compared with stable plaque group. (5) The levels of miR-21 and miR-146a in PBMCs and plasma were significantly higher in soft plaque group than in fibrous plaque group and calcified plaque group. However, miR-155 in PBMCs and plasma was significantly lower in soft plaque group. CONCLUSIONS: The expression of miR-21 and miR-146a are associated with the plaque stability in coronary stenotic lesions, whereas miR-155 expression is inversely associated with the plaque stability.

Correlation between maternally expressed gene 3 expression and heart rate variability in heart failure patients with ventricular arrhythmia.

AIM: The aim of the study was to analyse the correlation between maternally expressed gene 3 (MEG3) expression and heart rate variability (HRV) in heart failure patients with ventricular arrhythmia (VA). METHODS: A total of 130 heart failure patients, treated from July 2018 to March 2021, were prospectively selected and divided into a non-VA group (n = 85) and a VA group (n = 45) according to the presence or absence of VA. The correlations of serum MEG3 expression and HRV with cardiac function indicators were investigated by Pearson correlation analysis. Receiver operating characteristic (ROC) curves were plotted to assess the predictive value of MEG3, HRV and their combination for the occurrence of heart failure complicated with VA. RESULTS: The VA group had a higher left atrial diameter (LAD) and left ventricular end-diastolic diameter (LVEDD) but lower left ventricular ejection fraction (LVEF) and ratio of mitral early diastolic peak velocity (E) to late peak atrial filling velocity (A) (E/A) than the non-VA group (p < 0.05). The serum MEG3 expression was negatively correlated with: standard deviation of the average RR intervals calculated over five-minute segments in the 24-hour record (SDANN), SDANN index, standard deviation of normal-to-normal RR interval (SDNN) index, percentage of differences between adjacent normal RR intervals exceeding 50 ms (PNN50), root mean square of successive difference (RMSSD), low frequency (LF), high frequency (HF), very low frequency (VLF), LVEF and E/A (r < 0, p < 0.05). The serum MEG3 expression was positively correlated with LAD and LVEDD (r > 0, p < 0.05). The areas under the ROC curves of MEG3, SDANN, SDANN index, SDNN index, PNN50, RMSSD, LF, HF, VLF and their combination for the prediction of the occurrence of heart failure complicated with VA were 0.812, 0.731, 0.737, 0.689, 0.860, 0.783, 0.791, 0.856, 0.769 and 0.966, respectively. CONCLUSION: MEG3 combined with HRV can effectively predict the occurrence of heart failure complicated with VA.

miR-155 inhibits oxidized low-density lipoprotein-induced apoptosis in different cell models by targeting the p85α/AKT pathway.

The apoptosis of vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), and macrophages directly causes the instability or rupture of atherosclerotic plaques. Accumulating evidence suggests that oxidized low-density lipoprotein (OxLDL) could induce apoptosis via endogenous or exogenous pathways. Interestingly, it has been reported that microRNA155 (miR-155) plays a pivotal role in the regulation of apoptosis. Here, we hypothesized that overexpression of miR-155 could inhibit OxLDL-induced apoptosis by targeting the p85α/AKT pathway. In this study, we established models of OxLDL-induced apoptosis in mouse VECs, VSMCs, and macrophages. Furthermore, we explored the effects of miR-155 expression on the apoptosis of different cells, and ultimately revealed whether miR-155 regulated apoptosis by targeting the p85α/AKT pathway. The results demonstrated that miR-155 inhibited p85α expression and attenuated VEC, VSMC, and macrophage apoptosis, at least in part by suppressing the expression of p85α-activated AKT to inhibit apoptosis. Our findings collectively suggested that miR-155 attenuated OxLDL-mediated apoptosis in different cells by targeting p85α, supporting its possible therapeutic role in atherosclerosis.