Brain natriuretic Peptide production and secretion in inflammation

Tsuneo Ogawa1, Adolfo J de Bold

  • 1Cardiovascular Endocrinology Laboratory, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, ON, Canada K1Y 4W7.

Journal of Transplantation
|December 20, 2012
PubMed

Insights

Inflammation selectively increases brain natriuretic peptide (BNP) in cardiac disorders, unlike atrial natriuretic factor (ANF). This finding offers insights into cardiac inflammation and BNP regulation.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Immunology

Background:

  • Cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are upregulated in cardiac disorders.
  • Hemodynamic and neuroendocrine changes are key in cardiac disease progression.
  • Acute cardiac allograft rejection elevates plasma BNP but not ANF.

Purpose of the Study:

  • To investigate the selective regulation of BNP gene expression by inflammatory substances.
  • To understand the differential response of ANF and BNP to inflammation in cardiac conditions.

Main Methods:

  • Utilized cardiomyocyte cultures to study the effects of cytokines (TNFα and IL-1β) on ANF and BNP expression.
  • Observed in vivo changes in plasma BNP levels during acute cardiac allograft rejection, sepsis, and acute myocarditis.

Main Results:

  • Cytokines TNFα and IL-1β selectively stimulated cardiac BNP at transcriptional and translational levels in vitro.
  • ANF expression was unaffected by these cytokines in cardiomyocyte cultures.
  • Elevated plasma BNP levels were observed in vivo during acute cardiac allograft rejection, sepsis, and acute myocarditis, correlating with inflammation.

Conclusions:

  • Inflammation, mediated by cytokines, selectively upregulates BNP gene expression and secretion in cardiomyocytes.
  • This selective BNP response to inflammation is a significant factor in specific cardiac conditions like allograft rejection, sepsis, and myocarditis.
  • BNP may serve as a more specific biomarker for inflammation-driven cardiac events compared to ANF.

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