Abstract 15062: Heart-Failure Specific MicroRNAs: Comparison Between Patients and Murine Model
Purpose: Circulating microRNAs (miRNAs) have been proposed as biomarkers of several cardiac diseases, including myocardial infarction and Heart Failure (HF). In a preliminary expression profile screening, we have identified 10 miRNAs as potentially deregulated in plasma of HF patients. Here, we examined the expression pattern of these miRNAs both in plasma and cardiac samples from a murine model of HF. The aim of the work was to validate these potential biomarkers in a murine model of the disease.
Methods: The expression of 10 potentially HF-regulated-miRNAs (miR-1, -124a, -133a, -154, -299-5p, -379, -423-5p, -451, -499-5p, and -654-5p) was examined by qRT-PCR in plasma and heart samples from mice that underwent Thoracic Aortic Constriction (TAC) obtained by banding to induce HF. Disease insurgence was verified by echocardiography. Plasma and left ventricle specimens (n = 5/group) were collected both from operated and sham animals eight weeks after intervention.
Results: Among investigated plasmatic miRNAs, only miR-1 and -133a exhibited a positive regulation in TAC-mice (10.6 and 11.9 fold increase, respectively, compared to controls, p<0.05). This is consistent with our previous results and literature regarding HF patients. Intriguingly, in cardiac tissue samples of failing mice, miR-1 showed a decrease (-4.3), while miR-654-5p demonstrated to be positively regulated (2.5 fold increase) by TAC (p<0.05 for both comparisons). No other significant difference was observed between HF and control mice.
Conclusions: Our results suggest that miR-1 and miR-133a may be regarded as potentially useful biomarkers for HF, as we found them regulated both in patient and murine plasma. An interesting observation is that miR-1 expression showed an opposing modulation in plasma and heart from HF-mice. This finding suggests a possible active release from the HF heart. The limited overlap between human and mouse plasma could be due to the differences in terms of HF severity, treatment, and progression of the disease during the lifespan of the affected subjects.
Author Disclosures: Y. D’Alessandra: None. A.P. Beltrami: None. M. Carena: None. P. Devanna: None. D. Cesselli: None. M.C. Capogrossi: None. M. Musumeci: None. G. Pompilio: None. G.I. Colombo: None.
- © 2014 by American Heart Association, Inc.