MicroRNA-363-3p serves as a diagnostic biomarker of acute myocardial infarction and regulates vascular endothelial injury by targeting KLF2

Abstract

Background: Acute myocardial infarction (AMI) is a serious cardiovascular disease. This study aimed to investigate the diagnostic value of in AMI patients and explore the effects of miR-363-3p on vascular endothelial injury in an AMI rat model. Methods:The Expression of miR-363-3p was measured by quantitative real-time PCR. A receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic value of miR-363-3p in AMI patients. The biomarkers of endothelial injury were estimated using enzyme-linked immunosorbent assays, and the correlation of miR-363-3p with these markers was assessed. AMI rat model was constructed using coronary artery ligation, and the effects of miR-363-3p on endothelial injury and endothelial cell proliferation were analyzed.Results: Serum expression of miR-363-3p was upregulated in the AMI patients compared with healthy controls. The increased serum miR-363-3p serves a candidate diagnostic biomarker of AMI. The correlation analysis indicated that serum miR-363-3p expression was positively correlated with the concentration of endothelial injury biomarkers in AMI patients. Furthermore, the increased endothelial injury biomarkers in AMI rats were all inhibited by the knockdown of miR-363-3p, and the cell proliferation of human umbilical vein endothelial cells was obviously enhanced by the reduction of miR-363-3p. The prediction resultsshown that Kruppel-like factor 2 (KLF2) is a target of miR-363-3p, and their interaction was proved using a luciferase reporter assay.Conclusions: Collectively, overexpression of miR-363-3p acts as a diagnostic biomarker for patients with AMI, and the downregulation of miR-363-3p improves AMI-associated endothelial injury by targeting KLF2, which indicated that miR-363-3p has a potential to develop the treatment of AMI.

Circulating MicroRNAs predict glycemic improvement and response to a behavioral intervention

“…MiR let-7c is as a potential therapeutic target to mediate the activity of transforming growth factor β1 ( TGF- β 1 ) in diabetic kidney disease and [ 31 ] and polarization of macrophages in immune responses [ 32 ]. MiR-186, [ 33 ] miR-342, [ 34 ] miR-363, [ 35 ] miR-374, [ 36 ] and miR-92a [ 37 ] have been identified in studies of vascular endothelial cell function and therefore may be more related to complications from, rather than the etiology of, T2DM. Similarly, miR-296 appears to target sodium-glucose transporter-2 ( SGLT2 ) to promote wound healing in individuals with T2DM [ 38 ].…”

The Involvement of Krüppel-like Factors in Cardiovascular Diseases

“…As confirmed in rat studies with knockdown of miR-363-3p, which showed that endothelial injury biomarkers are reduced. In the same study, they observed that the activity of KLF-2 was inhibited with the upregulation of miR-363-3p, leading patients towards a higher probability of suffering AMI [110].…”

Exosomal miRNA Profile in Small-for-Gestational-Age Children: A Potential Biomarker for Catch-Up Growth

“…This adversely affects cell proliferation whereas overexpression suppresses tumor formation [ 27 , 28 , 29 ]. The miRNA miR-363-3p is associated with various diseases and its overexpression decreases cell proliferation [ 30 , 31 , 32 ]. Recently, miR-363-3p was shown to have suppressive effects on neonatal hypoxic ischemic encephalopathy [ 33 ].…”