Grażyna Sygitowicz1, Mariusz Tomaniak2, Olga Błaszczyk3, Łukasz Kołtowski2, Krzysztof J Filipiak2, Dariusz Sitkiewicz4. 1. Department of Laboratory Medical Diagnostics, Medical University of Warsaw, Warsaw, Poland. Electronic address: gsygitowicz@poczta.onet.pl. 2. 1st Chair and Department of Cardiology, Medical University of Warsaw, Warsaw, Poland. 3. Department of Pharmacogenomics, Medical University of Warsaw, Warsaw, Poland. 4. Department of Laboratory Medical Diagnostics, Medical University of Warsaw, Warsaw, Poland.
Abstract
BACKGROUND: Cardiomyocytes produce a wide variety of bioactive molecules that regulate numerous physiological and pathophysiological processes. Recently, it has been recognized that changes in microribonucleic acid (miRNA) expression may lead to cardiac dysfunction. AIMS: To assess the expression of circulating miRNAs (miR-1, miR-21 and miR-208a) in patients with symptomatic heart failure (HF), and to investigate the relationship between expression of these miRNAs and secretion of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and galectin-3. METHODS: Thirty-five patients in New York Heart Association (NYHA) class II/III (age: 68.8 ± 13.0 years) and 26 patients in NYHA class IV (age: 72.0 ± 10.4 years) hospitalized in the intensive coronary care unit participated in the study. Serum concentrations of miRNAs were measured by quantitative real-time polymerase chain reaction. Basic biochemical assays were carried out, and NT-proBNP and galectin-3 concentrations were measured in all serum samples. RESULTS: miR-1 was downregulated in patients with symptomatic HF and its expression decreased with severity of NYHA class (P=0.007). In contrast, overexpression of miR-21 was seen in all patients, independent of HF severity. Results suggest no miR-208a leakage into the circulation in patients with symptomatic HF. There was an inverse relationship between miR-1 expression and NT-proBNP concentration (Spearman's rank correlation coefficient [r]=-0.389; P=0.023) in patients in NYHA class II/III. Overexpression of miR-21 correlated significantly with galectin-3 concentration (r=0.422; P=0.032). CONCLUSION: Dysregulation of miR-1 and miR-21 expression may be essential for the development of HF; miR-1 might become a biomarker for predicting HF exacerbation.
BACKGROUND: Cardiomyocytes produce a wide variety of bioactive molecules that regulate numerous physiological and pathophysiological processes. Recently, it has been recognized that changes in microribonucleic acid (miRNA) expression may lead to cardiac dysfunction. AIMS: To assess the expression of circulating miRNAs (miR-1, miR-21 and miR-208a) in patients with symptomatic heart failure (HF), and to investigate the relationship between expression of these miRNAs and secretion of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and galectin-3. METHODS: Thirty-five patients in New York Heart Association (NYHA) class II/III (age: 68.8 ± 13.0 years) and 26 patients in NYHA class IV (age: 72.0 ± 10.4 years) hospitalized in the intensive coronary care unit participated in the study. Serum concentrations of miRNAs were measured by quantitative real-time polymerase chain reaction. Basic biochemical assays were carried out, and NT-proBNP and galectin-3 concentrations were measured in all serum samples. RESULTS:miR-1 was downregulated in patients with symptomatic HF and its expression decreased with severity of NYHA class (P=0.007). In contrast, overexpression of miR-21 was seen in all patients, independent of HF severity. Results suggest no miR-208a leakage into the circulation in patients with symptomatic HF. There was an inverse relationship between miR-1 expression and NT-proBNP concentration (Spearman's rank correlation coefficient [r]=-0.389; P=0.023) in patients in NYHA class II/III. Overexpression of miR-21 correlated significantly with galectin-3 concentration (r=0.422; P=0.032). CONCLUSION: Dysregulation of miR-1 and miR-21 expression may be essential for the development of HF; miR-1 might become a biomarker for predicting HF exacerbation.
Authors: Carmen C Sucharov; David P Kao; J David Port; Anis Karimpour-Fard; Robert A Quaife; Wayne Minobe; Karin Nunley; Brian D Lowes; Edward M Gilbert; Michael R Bristow Journal: JCI Insight Date: 2017-01-26
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