Abstract
The primary objective of this study investigated the role of microRNA-320 (miR-320) on left ventricular remodeling in the rat model of myocardial ischemia-reperfusion (I/R) injury, and we intended to explore the myocardial mechanism of miR-320-mediated myocardium protection. We collected 120 male Wistar rats (240–280 g) in this study and then randomly divided them into three groups: (1) sham surgery group (sham group: n = 40); (2) ischemia-reperfusion model group (I/R group: n = 40); and (3) I/R model with antagomir-320 group (I/R + antagomir-320 group: n = 40). Value changes of heart function in transesophageal echocardiography were recorded at various time points (day 1, day 3, day 7, day 15 and day 30) after surgery in each group. Myocardial sections were stained with hematoxylin and eosin (H&E) and examined with optical microscope. The degree of myocardial fibrosis was assessed by Sirius Red staining. Terminal dUTP nick end-labeling (TUNEL) and qRT-PCR methods were used to measure the apoptosis rate and to determine the miR-320 expression levels in myocardial tissues. Transesophageal echocardiography showed that the values of left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP) and ±dp/dtmax in the I/R group were obviously lower than those in the sham group, while the left ventricular end-diastolic pressure (LVEDP) value was higher than that in the sham group. The values of LVEF, LVFS, LVSP and ±dp/dtmax showed a gradual decrease in the I/R group, while the LVEDP value showed an up tendency along with the extension of reperfusion time. The H&E staining revealed that rat myocardial tissue in the I/R group presented extensive myocardial damage; for the I/R + antagomir-320 group, however, the degree of damage in myocardial cells was obviously better than that of the I/R group. The Sirius Red staining results showed that the degree of myocardial fibrosis in the I/R group was more severe along with the extension of the time of reperfusion. For the I/R + antagomir-320 group, the degree of myocardial fibrosis was less severe than that in the I/R group. Tissues samples in both the sham and I/R + antagomir-320 groups showed a lower apoptosis rate compared to I/R group. The qRT-PCR results indicated that miR-320 expression in the I/R group was significantly higher than that in both the sham and I/R + antagomir-320 groups. The expression level of miR-320 is significantly up-regulated in the rat model of myocardial I/R injury, and it may be implicated in the prevention of myocardial I/R injury-triggered left ventricular remodeling.
Highlights
Cardiovascular disease is the leading cause of death in both the United States and among worldwide populations, according to the World Health Organization [1]
Transesophageal echocardiography was applied to detect cardiac function in the sham group, the I/R group and the I/R + antagomir-320 group based on the left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), LVSP, left ventricular end-diastolic pressure (LVEDP) and
The result has shown no significant differences of LVEF, LVFS, LVSP, LVEDP and ±dp/dtmax at different time points in the sham group
Summary
Cardiovascular disease is the leading cause of death in both the United States and among worldwide populations, according to the World Health Organization [1]. Ischemic heart disease (IHD) is classified as the leading cause of global mortality by the Global Burden of Disease study from various types of cardiovascular diseases [2]. I/R injury may be involved in the development of left ventricular remodeling associated with cardiac myocyte death, vascular rarefaction, fibrosis, inflammation and electrophysiological remodeling, resulting in the pathophysiology of advancing heart failure and sudden cardiac death [5,6,7,8]. Recent investigations found molecular and cellular mechanisms and suggested that microRNAs (miRs) may be crucial in the regulation of I/R injury-induced cardiac injury and dysfunction, governing the development of ventricular remodeling after I/R injury [9,10,11]
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