Patients with rheumatic heart disease (RHD) and atrial fibrillation (AF) often have a risk of intracardiac thrombosis. Exfoliated thrombus is easy to cause embolic diseases. This study revealed the risk of intracardiac thrombosis in patients with RHD with AF by exploring the expression of plasma microRNA miR-145. The expression of plasma miR-145 in 58 patients with RHD complicated with AF was detected by real-time quantitative polymerase chain reaction [28 cases in thrombus (TH) group and 30 cases in non-thrombus (NTH) group]. At the same time, a healthy control group (33 cases) was established. The correlation between miR-145 and thrombosis in RHD was analyzed. The expression of plasma miR-145 in TH group and NTH group decreased significantly, especially in TH group (P < .01). In TH group and NTH group, the expression of miR-145 was negatively correlated with D-Dimer level, Factor XI concentration and tissue factor level as well as left atrial diameter (all P < .01, respectively). The receiver operating curve analysis showed that the expression of miR-145 had diagnostic significance for RHD and its intracardiac thrombosis. In this study, we suggest that the change of plasma miR-145 expression in patients with RHD is related to coagulation activity and fibrinolysis, which can predict the risk of intracardiac thrombosis.

Objectives: Differential expression of microRNAs (miRNAs) has been confirmed to promote hypertrophic scar (HS) formation. However, this mechanism remains to be further elucidated. This paper investigated the effects of microRNA26a on HS of rabbit ears or its mechanism. Methods: The rabbit HS models were established and randomly assigned to either the experimental group (20 rabbits with treatment through triamcinolone acetonide) or the scar group (20 rabbits without treatment). In addition, 10 unmodeled rabbits were served as control group. The expression of microRNA-26a in HS tissues was detected via a stem-loop real-time polymerase chain reaction (RT-PCR). Results: According to RT-PCR, we showed the decreased expression of microRNA-26a in the scar group compared with that in the experimental group, and in the experimental group compared with that in the control group ( p < .01). In addition, the expression of microRNA-26a was negatively correlated with scar thickness (STs), number of fibroblasts (NFs), Collagen I (Col I) level, Collagen III (Col III) level, Interleukin-6 (IL-6) level, and Tumor necrosis factor-alpha (TNF-α) level (all p < .01). Conclusions: Our findings revealed that the increase of microRNA-26a expression might alleviate excessive inflammation during the HS formation, inhibit fibroblast proliferation and collagen deposition in HS, and promote the treatment of HS.