C-type natriuretic peptide transcriptomic profiling increases in human leukocytes of patients with chronic heart failure as a function of clinical severity

The aim of this study was to evaluate the transcriptomic profiling of C-type natriuretic peptide (CNP) and of its specific receptor, NPR-B in human leukocytes of heart failure (HF) patients as a function of clinical severity, assessing the possible changes with respect to healthy subjects (C). mRNA expression was evaluated by Real-Time PCR and total RNA was extracted from leukocytes of C (n = 8) and of HF patients (NYHA I-II, n = 7; NYHA III-IV, n = 13) with PAXgene Blood RNA Kit. Significantly higher levels of CNP mRNA expression were found in HF patients as a function of clinical severity (C = 0.23 ± 0.058, NYHA I-II = 0.47 ± 0.18, NYHA III-IV = 2.58 ± 0.71, p = 0.005 C vs NYHA III-IV, p = 0.017 NYHA I-II vs NYHA III-IV) and NPR-B transcript levels resulted down-regulated in HF patients with higher NYHA class (C = 2.2 ± 0.61, NYHA I-II = 2.76 ± 0.46, NYHA III-IV = 0.29 ± 0.13, p = 0.001 C vs NYHA III-IV, p < 0.0001 NYHA I-II vs NYHA III-IV). A significant negative correlation between CNP and NPR-B mRNA expression (r = 0.5, p = 0.03) was also observed. These results suggest a co-regulation of NPR-B and CNP expression supporting the relevance of this receptor in human disease characterized by a marked inflammatory/immune component and suggesting the possibility of manipulating inflammation via pharmacological agents selective for this receptor.