Elevated plasma levels of miR-29a are associated with hemolysis in patients with hypertrophic cardiomyopathy
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,...
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Published in | Clinica chimica acta Vol. 471; pp. 321 - 326 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.08.2017
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Subjects | |
Online Access | Get full text |
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Summary: | 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.
miR-29a expression was evaluated in plasma (n=50) and myocardial samples (n=4) from patients with hypertrophic cardiomyopathy using RT-qPCR.
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.
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.
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•miR-29a was highly expressed in the myocardium•miR-29a in the plasma is in a extravesicular protein bound form.•The turbulent flow in the outflow tract in patients with hypertrophic cardiomyopathy leads to intravascular hemolysis•Plasma miR-29a was identified to be changing with increased hemolysis (intravascular or during sample collection) and not with myocardial damage.•Hemolysis and platelet activation during sample collection and handling are potential sources of preanalytical errors |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0009-8981 1873-3492 |
DOI: | 10.1016/j.cca.2017.07.004 |