Abstract
Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play a role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential role of miR-187 in cardiac I/R injury and its underlying mechanisms. miR-187 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor to confirm the function of miR-187 in H/R. DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with DYRK2 inhibitor. A myocardium I/R mouse model was established. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.
Highlights
Myocardial infarction is a serious representation of cardiovescular disease, ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries
These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of Dual specificity tyrosine phosphorylation regulated kinase 2 (DYRK2) expression
The results indicated that miR-187 may be a potential regulator in the protective effect of H/R-induced cardiomyocyte apoptosis
Summary
Myocardial infarction is a serious representation of cardiovescular disease, ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries. Myocardial infarction is a serious representation of cardiovescular disease that refers to a series of symptoms such as acute occlusion of the coronary arteries[1]. The process of choosing a set of optimal characteristic to categorize normal and myocardial infarction ECG signals is difficult and can be misinterpreted. Ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries, which can cause injury to the cardiomyocytes. The major mechanisms of I/R contribute to cardiomyocyte injury caused by the overexpression of proinflammatory cytokines by immunological cells[6], reactive oxygen species (ROS) generation[7], Ca2+ overload[8], and apoptosis[9]
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