The effect of myocardial infarction-associated transcript 2 (Mirt2) and miR-101 on sepsis-induced myocardial injury in rats.

ABSTRACT

OBJECTIVE: The aim of this study was to explore the effect of myocardial infarction associated transcript 2 (Mirt2) and miR-101 on sepsis-induced myocardial injury in rats and its mechanism. MATERIALS AND METHODS: Sprague Dawley (SD) rats were divided into sham group, CLP group, CLP + adeno-associated virus (AAV)-lncRNA Mirt2 group, CLP + AAV-NC group and CLP + AAV-lncRNA Mirt2 + agomiR-101 group. Rat CLP model was constructed. PanoViewb1500 was used to detect left ventricular systolic blood pressure (LVSP), left ventricular end diastolic blood pressure (LVEDP), ejection fraction (EF) and fraction shortening (FS) values. Thereafter, Mirt2 and miR-101 expression levels were detected by real-time polymerase chain reaction (RT-PCR), myocardial pathological damage was detected by hematoxylin-eosin (HE) staining, and Interleukin-1ß (IL-1ß) expression was by immunohistochemical staining. Next, enzyme linked immunosorbent assay (ELISA) was performed to detect the levels of serum inflammatory factors, tumor necrosis factor α (TNF-α), IL-1ß, Interleukin-6 (IL-6), myeloperoxidase (MPO), cardiac troponin I (cTn I) and creatine kinase isoenzyme (CK-MB). After that, Western blot was used to detect the expression of inflammatory factors and Phosphatidylinositol-3-kinases (PI3K)/protein-serine-threonine kinase (AKT) signaling pathway. Finally, Dual-Luciferase reporter gene assay was conducted to detect the relationship between Mirt2 and miR-101. RESULTS: Compared with those in the sham group, the cardiac function of the rats in the CLP group was significantly deteriorated, the cardiac structure was disordered, and the expression of pro-inflammatory related factors was significantly increased. Compared with those in CLP group, the cardiac function of the CLP + AAV-lncRNA Mirt2 group was alleviated, the PI3K/AKT signaling pathway was activated, the cardiac structure was slightly disordered, and the expression of pro-inflammatory related factors was reduced. To some extent, miR-101 could directly inhibit the effect of Mirt2. CONCLUSIONS: Mirt2 can silence miR-101 and inhibit myocardial inflammatory response in sepsis rats through the PI3K/AKT signaling pathway, thus improving cardiac structure and function.