Purpose: Myocardial ischemia-reperfusion injury primarily causes myocardial infarction (MI), which is manifested by cell death. Angiogenesis is essential for repair and regeneration in cardiac tissue after MI. In this study, we aimed to investigate the effect of exosomes derived from the serum of MI patients in angiogenesis and its related mechanism. Patients and Methods: Exosomes, isolated from serum, were collected from MI (MIexosome) and control (Con-exosome) patients. After coculturing with human umbilical vein endothelial cells, MI-exosome promoted cell proliferation, migration, and tube formation. Results: The results revealed that the production and release of MI-exosome were associated with cardiomyocytes. Moreover, microarray assays demonstrated that miRNA-143 was significantly decreased in MI-exosome. Meanwhile, the overexpression and knockdown of miRNA-143 could inhibit and enhance angiogenesis, respectively. Furthermore, the effect of exosomal miRNA-143 on angiogenesis was mediated by its targeting gene, insulin-like growth factor 1 receptor (IGF-IR), and was associated with the production of nitric oxide (NO). Conclusion: Taken together, exosomes derived from the serum of patients with MI promoted angiogenesis through the IGF-IR/NO signaling pathway. The results provide novel understanding of the function of exosomes in MI.

Timely prediction of the risk of heart failure in acute myocardial infarction patients is critical for better prognosis. This article aims to evaluate the predictive value of serum soluble growth stimulation expressed gene 2 (sST2) and interleukin-33 in patients with acute myocardial infarction complicated by heart failure. A total of 42 healthy controls and 144 acute myocardial infarction patients were recruited in the study. According to Killip cardiac function classification as the basis for concurrent heart failure, they were distributed into non-heart failure group ( n = 76) and heart failure group ( n = 68). ELISA was utilized to determine the serum sST2 and interleukin-33 levels, and the diagnostic efficiency was evaluated by receiver operating characteristics curve. sST2 and interleukin-33 levels in patients with acute myocardial infarction were significantly increased when compared with normal healthy controls, and were further enhanced in the heart failure group. With the increased Killip cardiac function classification, interleukin-33 and sST2 levels were gradually elevated. Multivariate analysis indicated that interleukin-33 and sST2 could be used as independent predictors for heart failure combined with acute myocardial infarction.

Globally, acute myocardial infarction (AMI) is a serious condition affecting millions of individuals. While AMI therapy improves blood flow during surgery, reperfusion-induced injury may also occur, leading to secondary cardiac damage or even death. Here, we investigated miR-129-5p in myocardial ischemia-reperfusion (I/R) injury in rats, to explore reperfusion-related molecular mechanisms in myocardium. We used Sprague Dawley rats to establish a myocardial I/R model, with agomiR-129-5p injection, and used rat cardiomyocytes (H9c2) treated with anoxia-reoxygenation (A/R) to mimic myocardial I/R injury in vitro. A dual-luciferase reporter assay determined miR-129-5p binding to high mobility group box-1 (HMGB1) in H9c2 cells. We showed that exogenous miR-129-5p restored cardiac function indices, alleviated cardiac injury, relieved inflammatory effects and reduced infarct size and cell apoptosis in rat myocardium after I/R treatment. Elevated miR-129-5p induced a reduction in HMGB1 expression in rat I/R myocardium. miR-129-5p also targeted HMGB1, and negatively regulated its expression in H9c2 cells. Moreover, miR-129-5p overexpression in the cardiomyocytes reduced cell apoptosis and recovered cell viability after A/R injury, which was reversed by subsequent HMGB1 overexpression. These findings suggest miR-129-5p plays a cardioprotective role in ameliorating myocardial I/R injury in rats, by negatively targeting HMGB1. This mechanism provides new insights into the treatment of myocardium reperfusion-related damage.

Accumulating evidence shows that long non-coding RNAs (lncRNAs) are widely involved in cellular processes of myocardial ischemia/reperfusion (I/R). The present study investigated the functions of lncRNA SNHG16 in myocardial I/R and the mechanism mediated by SNHG16. The myocardial I/R rat and cell model and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established to detect the expression of SNHG16. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Myocardial cell apoptosis was assessed by TUNEL staining. Dual-luciferase gene reporter was applied to determine the interaction between the molecules. The expressions of SNHG16 were upregulated in myocardial I/R injury models. Inhibition of SNHG16 relieved myocardial I/R injury in vivo and in vitro silencing of SNHG16 alleviated H/R induced cardiomyocyte apoptosis. To explore the regulatory mechanism, it was discovered that SNHG16 directly interacted with miR-183, while forkhead box O1 (FoxO1) was a target of microRNA (miR)-183. Findings from rescue assays revealed that miR-183 inhibitor and upregulation of FOXO1 can rescue the effect of sh-SNHG16 on H/R-induced cardiomyocyte apoptosis. The results indicated that the lncRNA SNHG16/miR-183/FOXO1 axis exacerbated myocardial cell apoptosis in myocardial I/R injury, suggesting SNHG16 as a potential therapeutic target for myocardial I/R injury.

Although a few microRNAs (miRNAs) are involved in the regulation of myocardial ischemia/reperfusion injury (MI/RI), their exact roles in this process, and the mechanisms involved have not been fully elucidated. This study was carried out to investigate the protective effects of miR-34b and miR-337 against MI/RI. For this purpose, 56 Sprague-Dawley (SD) rats were randomly divided into two groups: sham operation group and myocardial MI/RI group, with 28 rats in each group. Then, a rat model of MI/RI was established. Changes in myocardial tissues of the two groups were determined using hematoxylin-Eosin (H&E) staining. Serum level of myocardial troponin c(TnT) was assayed with ELISA method, while myocardial tissue mRNA expressions of miR in the two groups was determined with qRT-PCR. Results showed that the rat model of MI/RI was successfully established, as was evident in myocardial cell necrosis, disorganized myocardial fibers, interstitial edema, and neutrophil infiltration. There were significant increases in serum troponin content and mRNA expression levels of miR-337 and miR-34b in tissues. In conclusion, the expression levels of miR-337 and miR-34b are increased in myocardial tissues of rats with MI/RI. Thus, miR-337 and miR-34b may be involved in the pathogenesis of MI/RI via regulation of NOX4 and Samd7, respectively. Finally, by using liposomal nanocarrier, the therapeutic effect of miR-337 and miR-34b on MI/RI was investigated.