Potential Involvement of MiR-30e-3p in Myocardial Injury Induced by Coronary Microembolization via Autophagy Activation

Abstract

Background/Aims: Coronary microembolization (CME) can lead to no-reflow or slow reflow, which is one of the important reasons for loss of clinical benefit from myocardial reperfusion therapy. MicroRNAs and autophagy are heavily implicated in the occurrence and development of almost all cardiovascular diseases. Therefore, the present study was designed to investigate the role of miR-30e-3p and autophagy in CME-induced myocardial injury rat model. Methods: Sixty rats were randomly divided into six groups: sham, CME 1h,3h,6h,9h, and 12h (n = 10 per group). Our CME rat model was created by injecting polyethylene microspheres (42mm) into the left ventricle of the heart; the sham group was injected with same volume of normal saline. The cardiac function and serum cardiac troponin I (cTnI) level of each group was measured. HE staining and HBFP staining were used to evaluate the myocardial micro-infarction area of myocardium tissue samples. Then RT-qPCR and western blot were used to detect the expression of miR-30e-3p and, autophagy related protein LC3-II and p62, respectively. Transmission electron microscope (TEM) was used to identify autophagic vacuoles in tissue samples. Results: The cardiac function of the CME 6h,9h, and 12h groups were significantly decreased compared to the sham group (P < 0.05) and the cTnI level in each group were also significantly increased (P < 0.05). The expression of miR-30e-3p in the CME 6h, 9h and 12h group were decreased significantly compared with the sham group (P < 0.05). Meanwhile, the expression of autophagy related protein LC3-II decreased significantly and p62 increased significantly in the CME 9h and 12h group (P < 0.05). TEM images showed typical autophagic vacuoles for each of the CME groups. Conclusions: Myocardial miR-30e-3p is down regulated after CME and is accompanied by inhibited autophagy and decreased cardiac function. Therefore, miR-30e-3p may be involved in CME-induced cardiac dysfunction by regulating myocardial autophagy.

Dysregulations of MicroRNA and Gene Expression in Chronic Venous Disease

“…Downregulation of miR-30e-3p was previously observed in coronary microembolization and was associated with myocardial injury mediated by impairment of autophagy in cardiomyocytes [86]. Therefore, the downregulation of miR-30e-3p found in this study may be involved in vascular dysfunction related to the thrombosis in CVD.…”

COVID-19 Virulence in Aged Patients Might Be Impacted by the Host Cellular MicroRNAs Abundance/Profile

“…Some of the miRNAs targeting the COVID-19 genome showed low abundance (down-regulated) with some underlying conditions ( Table 7). For example, miR-15b-5p (Coronary artery disease) [37], miR-15a-5p (Kidney disease) [38], miR-520c-3p (obesity/diabetes) [39], miR-30e-3p (Myocardial Injury) [40], miR-23c (hepatocellular carcinoma) [41], miR-30d-5p (non-small cell lung cancer) [42], miR-4684-3p (colorectal cancer) 43], and miR-518a-5p (Gastrointestinal stromal tumors) [44] down-regulated in pathophysiological condition.…”

Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin‐Associated Cardiac MicroRNA Signature

“…Importantly, 17 of these miRNAs were the same as those that were increased in ZL-Rap (Table 1). Among these miRNAs, miR-30e-3p is shown to be suppressed by insulin [45]; however, another study showed that its suppression is associated with myocardial injury induced by coronary microembolization via autophagy activation [46]. Moreover, miR-92b-3p is shown to be suppressed by hypoxia [47], but its expression is elevated in the heart tissues of both Rap-treated groups.…”