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Clin Chim Acta. 2017 Aug;471:321-326. doi: 10.1016/j.cca.2017.07.004. Epub 2017 Jul 4.

Elevated plasma levels of miR-29a are associated with hemolysis in patients with hypertrophic cardiomyopathy.

Author information

1
Laboratory of Biological Chemistry, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece; First Department of Cardiology, AHEPA University Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
2
Laboratory of Histology and Embryology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
3
First Department of Cardiology, AHEPA University Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
4
St. Luke's Cardiac Surgery Institute, Thessaloniki, Greece.
5
Laboratory of Biochemistry, Department of Chemistry, Aristotle University of Thessaloniki, Thessaloniki, Greece.
6
Blood Centre, AHEPA University Hospital, Thessaloniki, Greece.
7
Laboratory of Biological Chemistry, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
8
Laboratory of Biological Chemistry, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece. Electronic address: tzimagio@med.auth.gr.

Abstract

BACKGROUND:

miR-29a is a small non-coding RNA that is known to repress collagen synthesis. Interestingly, elevated plasma miR-29a was reported to correlate with pronounced myocardial fibrosis in patients with hypertrophic cardiomyopathy. The objective of this study was to elucidate the origin of plasma miR-29a, and evaluate its significance as a biomarker.

METHODS:

miR-29a expression was evaluated in plasma (n=50) and myocardial samples (n=4) from patients with hypertrophic cardiomyopathy using RT-qPCR.

RESULTS:

Although miR-29a was highly expressed in the myocardium, miR-29a plasma levels did not show any correlation with serum troponin I levels (rs=-0.12, p=0.43), and the heart does not release significant amounts of miR-29a into the circulation via exosome secretion. Conversely, miR-29a was present in red blood cells, and plasma levels correlated significantly with markers of hemolysis: lactic dehydrogenase (rs=0.36, p=0.01) and the absorbance of oxyhemoglobin at 414nm (rs=0.39, p=0.006). Furthermore, the association between serum haptoglobin and the maximal blood flow velocity in the left ventricle outflow tract (rs=-0.42, p=0.008) indicated that intravascular hemolysis is a manifestation of the disease.

CONCLUSIONS:

miR-29a is highly expressed in myocardial tissue from patients with hypertrophic cardiomyopathy. In contrast, plasma miR-29a is primarily of nonmyocardial origin and is correlated significantly with the extent of hemolysis observed in these patients.

KEYWORDS:

Hemolysis; Hypertrophic cardiomyopathy; Left ventricle outflow tract obstruction; miR-29a; microRNA

PMID:
28684219
DOI:
10.1016/j.cca.2017.07.004
[Indexed for MEDLINE]

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