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Disease Markers
Volume 31, Issue 5, Pages 259-265
http://dx.doi.org/10.3233/DMA-2011-0827

MicroRNAs, Innate Immunity and Ventricular Rupture in Human Myocardial Infarction

Nina Zidar,1 Emanuela Boštjančič,2 Damjan Glavač,2 and Dušan Štajer3

1Institute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
2Department of Molecular Genetics, Institute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
3Centre for Intensive Internal Medicine, University Medical Centre, Ljubljana, Slovenia

Received 14 October 2011; Accepted 14 October 2011

Copyright © 2011 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

MicroRNAs are non-coding RNAs, functionioning as post-transcriptional regulators of gene expression. Some microRNAs have been demonstrated to play a role in regulation of innate immunity. After myocardial infarction (MI), innate immunity is activated leading to an acute inflammatory reaction. There is evidence that an intense inflammatory reaction might contribute to the development of ventricular rupture (VR) after MI.

Using real-time PCR, we analysed the expression of miR-146a, miR-150, and miR-155 in autopsy samples of infarcted heart tissue from 50 patients with MI (23 with VR and 27 without VR).

An altered expression of all three microRNAs was found in MI compared to the normal hearts. Comparing MI patients with VR and those without VR, we found miR-146a up-regulation, and miR-150 and miR-155 down-regulation in patients with VR.

In conclusion, our study demonstrated an altered expression of miR-146a, miR-150, and miR-155 in MI compared to the normal hearts. These microRNAs are involved in regulation of the innate immunity. Differential expression of these microRNAs in MI patients with VR in comparison to those without VR provides further evidence that innate immunity resulting in an intense inflammatory reaction plays an important role in the pathogenesis of VR after MI in humans.