After the isolation of C-type natriuretic peptide (CNP) from porcine brain tissue, both CNP and CNP mRNA have been identified in vascular endothelium and in cardiac, renal, skeletal, and reproductive tissues as well as in organs of the immune system and in a variety of blood cells. The aim of this study was to evaluate the transcriptomic profiling of 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 N YHA 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.
C-TYPE NATRIURETIC PEPTIDE TRANSCRIPTOMIC PROFILING INCREASES IN LEUKOCYTES OF PATIENTS WITH CHRONIC HEART FAILURE AS A FUNCTION OF CLINICAL SEVERITY
Cabiati M;Sabatino L;Caruso R;Verde A;Caselli C;Prescimone T;Giannessi D;Del Ry S
2013
Abstract
After the isolation of C-type natriuretic peptide (CNP) from porcine brain tissue, both CNP and CNP mRNA have been identified in vascular endothelium and in cardiac, renal, skeletal, and reproductive tissues as well as in organs of the immune system and in a variety of blood cells. The aim of this study was to evaluate the transcriptomic profiling of 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 N YHA 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
