Abstract

Ischaemia/reperfusion (I/R) injury will cause additional death of cardiomyocytes in ischaemic heart disease. Recent studies revealed that renalase was involved in the I/R injury. So, the myocardial tissue-specific knockdown mouse models were needed for the investigations of renalase. To establish the mouse models, intramyocardial injection of siRNAs targeting renalase was performed in mice. The wild distribution and high transfection efficiency of the siRNAs were approved. And the renalase expression was efficiently suppressed in myocardial tissue. Compared with the high cost, time consumption, and genetic compensation risk of the Cre/loxP technology, RNA interference (RNAi) technology is much cheaper and less time-consuming. Among the RNAi technologies, injection of siRNAs is safer than virus. And considering the properties of the I/R injury mouse models, the efficiency and durability of injection with siRNAs are acceptable for the studies. Altogether, intramyocardial injection of siRNAs targeting renalase is an economical, safe, and efficient method to establish myocardial tissue-specific renalase knockdown mouse models.

Highlights

  • Ischaemic heart disease is one of the most common coronary artery diseases [1,2,3]

  • We found that the red fluorescence of Cy3 is distributed wildly in the myocardial tissue of the left ventricle (LV) (Figure 2)

  • Increasing evidence has implicated the potential roles of renalase in ischaemic heart disease

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Summary

Introduction

Restoration of blood flow can improve the clinical outcomes [4, 5], but reperfusion after ischaemia will cause additional death of cardiomyocytes in a process known as I/R injury. Recent evidence has implicated the potential protective roles of renalase in cardiomyocytes in the process of I/R injury [6,7,8,9,10]. To investigate the function of renalase, the technology of gene knockdown or knockout will be used. Conventional gene knockdown or knockout animal models are systemic and non-organ-specific. It will always cause some unpredictable abnormalities in other organs beside the target ones, which will influence the phenotypes of the animal models. The animal models with organspecific gene knockdown or knockout will be a better choice

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