Abstract
MiR34 involvement in myocardial injury repair and ageing has been well documented in mouse model. Our aim was to establish whether the inhibition of miR34 expression through locked nucleic acid (LNA) could be used as a pharmacological intervention to enhance human heart repair. Cardiac progenitor cells were obtained by right atrial specimen collection during intraoperative procedures. Our analysis revealed a direct correlation between miR34 expression and patient age, and its silencing by LNA promoted the cardiac progenitor growth rate up to twofold ( ± 0.8). Our results confirmed the relevance of miR34a in human heart ageing, as previously demonstrated in mouse. Moreover, the decrease of miR34 expression in the cardiac progenitor cell population indicates its role in maintaining an undifferentiated status and consequently in a lower proliferation rate with the involvement of genes such as Notch-1, Numb, and p63.
Highlights
Cardiovascular diseases are the leading cause of death today[1]
A recent report has demonstrated that the miR34 downmodulation after myocardial infarction (MI) induces a functional recovery and an increase in the scar reduction in mice[7]
Boon et al.[7] have shown that miR34 is involved in cardiac aging and its downmodulation through locked nucleic acid (LNA) inhibition supports cardiac repair in mice after acute myocardial infarction (AMI)
Summary
Cardiovascular diseases are the leading cause of death today[1] (http://www.who.int/mediacentre/factsheets/fs310/ en/). The increasing lifespan in the developed countries requires more efforts to find new treatments for cardiac repair and regeneration. Acute myocardial infarction (AMI) is a prominent cause of cardiac morbidity and mortality. The irreversible loss of functional cardiomyocytes and the resulting scar formation frequently progress with persistent cardiac dysfunction, causing a physiological impairment. To achieve tissue repair after myocardial infarction (MI), have shown limited benefits in clinical trials in which intracoronary infusion of autologous cardiosphere-derived cells (CDCs) decreased scar size, and increased myocardial function[2]. Explanted cellular expansion raises relevant issues of safety conditions, manipulation
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