MicroRNAs (miRNAs) are a class of small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Recently, it was reported that miR-137, miR-124, and miR-184 were widely expressed in the central nervous system and were vital to neuronal regulation. In this study, we detected the circulating levels of miR-137, miR-124, and miR-184 in PD patients, and explored the potential role of miR-124, miR-137, and miR-184 in the diagnosis of PD. We further described the relationship between these miRNAs and PD with depression (PD-Dep). The study recruited 60 controls and 60 PD patients, which were further divided into two subgroups, PD with depression (PD-Dep, n = 24) and non-depressed group (PD-NDep, n = 36) according to Hamilton Rating Scale for Depression. Plasma levels of miR-137, miR-124, and miR-184 were detected by qRT-PCR. Receiver-operating characteristic (ROC) curve was used to evaluate miR-124 and miR-137 levels as potential diagnostic biomarkers for PD. The results demonstrated that there were no significant differences in levels of miR-184 between PD patients and controls (p > 0.05). However, miR-137 levels were increased significantly for PD patients compared to controls (p < 0.05), while miR-124 levels were down-regulated (p < 0.05). The areas under the ROC curve (AUC) of miR-137 and miR-124 were 0.707 (95% CI 0.615-0.789, p < 0.05) and 0.709 (95% CI 0.618-0.633, p < 0.05), respectively. Correlation analysis revealed that there was no relationship between these two miRNAs levels and UPDRS scores or H&Y stage. There were no significant differences in miR-137 and miR-124 levels between PD-Dep and PD-NDep (p > 0.05). Thus, plasma levels of miR-137 and miR-124 are associated with Parkinson's disease and might be potential biomarkers of the diagnosis of PD. There were no associations of plasma miR-137 and miR-124 with the severity of PD motor symptoms or PD-Dep.

Atherosclerosis is a chronic inflammatory disease associated with the development of plaques that can be converted into an acute clinical event by thrombosis or plaque rupture. Mesenchymal stem cells (MSCs) exhibit therapeutic effects for the treatment of various diseases, including atherosclerosis. In this study, we show that microRNA-145 (miR-145) is associated with atherosclerosis by microRNA sequencing and bioinformatics analysis. MSC-derived miR-145-rich exosomes could efficiently deliver miR-145 from MSCs to human umbilical vein endothelial cells (HUVECs). Treatment of miR-145-rich exosomes could downregulate JAM-A, inhibit migration in vitro , and reduce atherosclerotic plaque in vivo . Our study suggests that MSC-derived miR-145-rich exosomes have great potential for atherosclerosis prevention.

Background: Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation can induce the secretion of IL-1β and IL-18 and after promoting the development of atherosclerosis. MiR-155 is an important microRNA that modulates inflammation in atherosclerosis, but the role of miR-155 in the regulation of the NLRP3 inflammasome is still unknown.Methods: The atherosclerosis model was set up using ApoE −/− mice, and the lentiviral vector (LV) was used to interfere the expression of miR-155. HE stains was used for plaque morphology, immunohistochemistry (IHC) and western blot were used for protein expression quantification. We used oxidized low-density lipoprotein (ox-LDL) to incubate PMA-preprocessed THP-1 macrophages and detected NLRP3 inflammasome activation and ERK1/2 phosphorylation by western blot and Enzyme-linked immunosorbent assay.Results: HE stains showed that the intravascular plaques in the miR-155-up group were remarkably increased, compared with negative control (NC) group. Results of IHC showed that the expression of caspase-1 and IL-1β in the miR-155-up group was the highest of four groups, consist with the Western blot analysis. The results of in vitro experiment show that ox-LDL promoted NLRP3 inflammasome activation and ERK1/2 phosphorylation. Blocking the ERK1/2 pathway could inhibit ox-LDL-induced NLRP3 inflammasome activation. Moreover, we found that the overexpression of miR-155 promoted the activation of the ox-LDL-induced NLRP3 inflammasome, which could also be blocked by the ERK inhibitor U0126.Conclusions: MiR-155 aggravates the carotid AS lesion in ApoE −/− mice and exerts a regulatory effect on NLRP3 inflammasome activation in ox-LDL-induced macrophages via the ERK1/2 pathway.

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As an evolutionarily conserved metabolic process, autophagy is involved in the process of atherosclerosis (AS). MicroRNA-155 (miR-155), a multifunctional miRNA, plays an important role in many physiological and pathological conditions, including AS and autophagy. However, the effect of miR-155 on the regulation of autophagy in endothelial cells has not been reported to date. Therefore, the objective of our study was to investigate the role of miR-155 in autophagy induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs). Our results demonstrated that ox-LDL induced autophagy in HUVECs and increased the expression of miR-155 significantly. Overexpression of miR-155 improved autophagic activity, whereas low expression of miR-155 inhibited autophagic activity. Therefore, the data demonstrated that miR-155 has a modulating effect on the autophagy of vascular endothelial cells.