Brain Natriuretic Peptide Production and Secretion in Inflammation
Gene expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are simultaneously upregulated in various cardiac disorders such as congestive heart failure, ischemic heart disease, and hypertensive heart disease, in which hemodyn...
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Series: | Journal of Transplantation |
Online Access: | http://dx.doi.org/10.1155/2012/962347 |
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doaj-8df52635b81d4f76b8b2d629c986cc572020-11-25T01:08:52ZengHindawi LimitedJournal of Transplantation2090-00072090-00152012-01-01201210.1155/2012/962347962347Brain Natriuretic Peptide Production and Secretion in InflammationTsuneo Ogawa0Adolfo J. de Bold1Cardiovascular Endocrinology Laboratory, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, ON, K1Y 4W7, CanadaCardiovascular Endocrinology Laboratory, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, ON, K1Y 4W7, CanadaGene expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are simultaneously upregulated in various cardiac disorders such as congestive heart failure, ischemic heart disease, and hypertensive heart disease, in which hemodynamic or neuroendocrine changes are key components in the progression of disease. However, during acute cardiac allograft rejection, plasma BNP levels are increased but not those of ANF. Successful treatment of the rejection episode decreases the elevated plasma BNP to prerejection values suggesting that substances related to inflammation may selectively influence BNP gene expression. Indeed, cytokines such as TNFα and IL-1β selectively stimulate cardiac BNP at the transcriptional and translational levels in cardiomyocyte cultures without affecting ANF. This selective BNP increase is seen in vivo, in addition to acute cardiac allograft rejection, in several circumstances where inflammation significantly contributes to the pathogenesis of disease such as in sepsis and in acute myocarditis.http://dx.doi.org/10.1155/2012/962347 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Tsuneo Ogawa Adolfo J. de Bold |
spellingShingle |
Tsuneo Ogawa Adolfo J. de Bold Brain Natriuretic Peptide Production and Secretion in Inflammation Journal of Transplantation |
author_facet |
Tsuneo Ogawa Adolfo J. de Bold |
author_sort |
Tsuneo Ogawa |
title |
Brain Natriuretic Peptide Production and Secretion in Inflammation |
title_short |
Brain Natriuretic Peptide Production and Secretion in Inflammation |
title_full |
Brain Natriuretic Peptide Production and Secretion in Inflammation |
title_fullStr |
Brain Natriuretic Peptide Production and Secretion in Inflammation |
title_full_unstemmed |
Brain Natriuretic Peptide Production and Secretion in Inflammation |
title_sort |
brain natriuretic peptide production and secretion in inflammation |
publisher |
Hindawi Limited |
series |
Journal of Transplantation |
issn |
2090-0007 2090-0015 |
publishDate |
2012-01-01 |
description |
Gene expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are simultaneously upregulated in various cardiac disorders such as congestive heart failure, ischemic heart disease, and hypertensive heart disease, in which hemodynamic or neuroendocrine changes are key components in the progression of disease. However, during acute cardiac allograft rejection, plasma BNP levels are increased but not those of ANF. Successful treatment of the rejection episode decreases the elevated plasma BNP to prerejection values suggesting that substances related to inflammation may selectively influence BNP gene expression. Indeed, cytokines such as TNFα and IL-1β selectively stimulate cardiac BNP at the transcriptional and translational levels in cardiomyocyte cultures without affecting ANF. This selective BNP increase is seen in vivo, in addition to acute cardiac allograft rejection, in several circumstances where inflammation significantly contributes to the pathogenesis of disease such as in sepsis and in acute myocarditis. |
url |
http://dx.doi.org/10.1155/2012/962347 |
work_keys_str_mv |
AT tsuneoogawa brainnatriureticpeptideproductionandsecretionininflammation AT adolfojdebold brainnatriureticpeptideproductionandsecretionininflammation |
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1725181103018344448 |