Abstract

Acute coronary syndrome (ACS) is a heart disease with a high mortality rate. Recently, more and more evidence illustrated that microRNAs (miRNA) participated in regulating the occurrence of heart disease. This study aimed to detect the level of serum miR-320a-3p in patients with ACS, predict its possibility as a candidate gene for diagnosis, and explore its potential mechanism in the regulation of ACS. 139 ACS patients and 126 controls were recruited in this study. The expression level of miR-320a-3p was determined by qRT-PCR. The predictive value in ACS was assessed by receiver operating characteristic (ROC) curve. Enzyme-linked immunosorbent assay (ELISA) was used to measure the protein expression levels of inflammatory factors. The downstream targets of miR-320a-3p were verified by luciferase reporter gene assay. In ACS patients and rat models, the expression level of serum miR-320a-3p was significantly increased. ROC curve revealed that abnormal expression of miR-320a-3p was of diagnostic value for ACS. In an in vivo rat model, down-regulation of miR-320a-3p inhibited the production of von Willebrand factor (vWF), Heart fatty acid-binding protein (H-FABP), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). In other words, down-regulation of miR-320a-3p reduced rat vascular endothelial injury and inflammation. X-linked inhibitor of apoptosis protein (XIAP) was determined to be a direct target of miR-320a-3p. miR-320a-3p is useful for the diagnosis of ACS. Animal experiments confirmed that up-regulated miR-320a-3p promoted vascular endothelial injury and inflammatory response by targeting XIAP, thus promoting the development of ACS. MiR-320a-3p may be a new breakthrough in the diagnosis and treatment of ACS.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call