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Original Research

MicroRNAs miR-1, miR-133a, miR-133b and miR-208 Are Dysregulated in Human Myocardial Infarction

Boštjančič E.a · Zidar N.a · Štajer D.b · Glavač D.a

Author affiliations

aDepartment of Molecular Genetics,Institute of Pathology, Faculty of Medicine, University of Ljubljana, and bCentre for Intensive Internal Medicine, University Medical Centre, Ljubljana, Slovenia

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Cardiology 2010;115:163–169

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Article / Publication Details

First-Page Preview
Abstract of Original Research

Received: July 28, 2009
Accepted: October 12, 2009
Published online: December 21, 2009
Issue release date: April 2010

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 1

ISSN: 0008-6312 (Print)
eISSN: 1421-9751 (Online)

For additional information: https://www.karger.com/CRD

Abstract

Objectives: MicroRNAs (miRNAs) are noncoding single-stranded RNA molecules that regulate gene expression in physiological functions, development and disease. In recent studies, three miRNAs have been described as muscle or cardiac specific: miR-1, miR-133, and miR-208, being involved in heart development and disease; but there are limited data on their role in human myocardial infarction (MI). We therefore analyzed their expression in human MI. Methods: Autopsy samples of infarcted heart tissue from 50 patients with MI, 8 healthy trauma victims and 9 fetuses that died in utero were included. miRNAs miR-1, miR-133a/b and miR-208 were analyzed using quantitative real-time polymerase chain reaction. Results:miR-208 was upregulated, whereas miR-1 and miR-133a were downregulated in MI compared to healthy adult and fetal hearts. All four tested miRNAs were downregulated in fetal hearts compared to healthy adult hearts. Conclusions: Our study showed the involvement of muscle- and/or cardiac-specific miRNAs miR-1, miR-133a/b and miR-208 in human MI. The most significant finding was upregulation of miR-208 and downregulation of miR-1 and miR-133a in MI compared to healthy adult hearts. Some patterns of miRNA expression were similar in MI and fetal hearts, supporting the concept of cardiac gene reprogramming in the remodeling of the heart.

© 2009 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Original Research

Received: July 28, 2009
Accepted: October 12, 2009
Published online: December 21, 2009
Issue release date: April 2010

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 1

ISSN: 0008-6312 (Print)
eISSN: 1421-9751 (Online)

For additional information: https://www.karger.com/CRD


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