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Published on: July 25, 2019

C-type natriuretic peptide transcriptomic profiling increases in human leukocytes of patients with chronic heart

M Cabiati1, L Sabatino, R Caruso

  • 1CNR Institute of Clinical Physiology, Laboratory of Cardiovascular Biochemistry, Pisa, Italy.

Peptides
|August 6, 2013
PubMed

Insights

Heart failure patients show increased C-type natriuretic peptide (CNP) and decreased NPR-B receptor mRNA in leukocytes, correlating with disease severity. This suggests NPR-B

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Immunology

Background:

  • Heart failure (HF) involves complex pathophysiological mechanisms.
  • Leukocyte gene expression may reflect systemic disease processes.
  • C-type natriuretic peptide (CNP) and its receptor NPR-B play roles in cardiovascular homeostasis.

Purpose of the Study:

  • To investigate the expression of CNP and NPR-B mRNA in leukocytes of heart failure patients.
  • To correlate CNP and NPR-B expression with heart failure clinical severity (NYHA class).
  • To compare gene expression in heart failure patients versus healthy controls.

Main Methods:

  • Total RNA extraction from leukocytes using PAXgene Blood RNA Kit.
  • Quantitative mRNA expression analysis via Real-Time PCR.
  • Recruitment of healthy controls (n=8) and heart failure patients (NYHA I-II, n=7; NYHA III-IV, n=13).

Main Results:

  • CNP mRNA levels were significantly elevated in HF patients, increasing with NYHA class (p=0.005 vs C, p=0.017 vs NYHA I-II).
  • NPR-B transcript levels were significantly down-regulated in HF patients with higher NYHA class (p=0.001 vs C, p<0.0001 vs NYHA I-II).
  • A significant negative correlation (r=0.5, p=0.03) was observed between CNP and NPR-B mRNA expression.

Conclusions:

  • Leukocyte CNP and NPR-B mRNA expression are altered in heart failure patients, with changes related to disease severity.
  • Results suggest co-regulation of CNP and NPR-B, highlighting NPR-B's role in inflammatory/immune components of disease.
  • Potential for targeting NPR-B with pharmacological agents to modulate inflammation in heart failure.

Keywords:
BloodC-type natriuretic peptideHeart failureHuman leukocytesNatriuretic peptide receptorReal-Time PCRmRNA expression

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