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Article type: Research Article
Authors: Zidar, Nina | Boštjančič, Emanuela | Glavač, Damjan | Štajer, Dušan
Affiliations: Institute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia | Department of Molecular Genetics, Institute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia | Centre for Intensive Internal Medicine, University Medical Centre, Ljubljana, Slovenia
Note: [] Corresponding author: Nina Zidar, Institute of Pathology, Faculty of Medicine, University of Ljubljana, Korytkova 2, 1000 Ljubljana, Slovenia. Tel.: +386 1 543 7149; Fax: +386 1 543 7101; E-mail: nina.zidar@mf.uni-lj.si
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.
Keywords: Myocardial infarction, ventricular rupture, pathogenesis, inflammation, innate immunity, microRNA
DOI: 10.3233/DMA-2011-0827
Journal: Disease Markers, vol. 31, no. 5, pp. 259-265, 2011
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