Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 296, Issue 6, Pages H1804-H1810Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.01033.2008
Keywords
neuron-restrictive silencer factor; guanylyl cyclase-A; cardiomyopathy; sudden death
Funding
- Japan Society for the Promotion of Science
- Japanese Ministry of Health, Labor and Welfare
- Japan Heart Foundation/Pfizer Pharmaceuticals Inc.
- Grant on Cardiovascular Disease Research
- Japan Heart Foundation/Novartis
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Uehara Memorial Foundation
- Ichiro Kanehara Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Mitsubishi Foundation
- Suzuken Memorial Foundation
- Takeda Medical Research Foundation
- Kanae Foundation for the Promotion of Medical Science
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Yasuno S, Usami S, Kuwahara K, Nakanishi M, Arai Y, Kinoshita H, Nakagawa Y, Fujiwara M, Murakami M, Ueshima K, Harada M, Nakao K. Endogenous cardiac natriuretic peptides protect the heart in a mouse model of dilated cardiomyopathy and sudden death. Am J Physiol Heart Circ Physiol 296: H1804-H1810, 2009. First published April 3, 2009; doi:10.1152/ajpheart.01033.2008.-Ventricular myocytes are known to show increased expression of the cardiac hormones atrial and brain natriuretic peptide (ANP and BNP, respectively) in response to pathological stress on the heart, but their function during the progression of nonischemic dilated cardiomyopathy remains unclear. In this study, we crossed a mouse model of dilated cardiomyopathy and sudden death, which we generated by cardioselectively overexpressing a dominant-negative form of the transcriptional repressor neuron-restrictive silencer factor (dnNRSF Tg mice), with mice lacking guanylyl cyclase-A (GC-A), a common receptor for ANP and BNP, to assess the effects of endogenously expressed natriuretic peptides during progression of the cardiomyopathy seen in dnNRSF Tg mice. We found that dnNRSF Tg; GC-A(-/-) mice were born normally, but then most died within 4 wk. The survival rates among dnNRSF Tg; GC-A(+/-) and dnNRSF Tg mice were comparable, but dnNRSF Tg; GC-A(+/-) mice showed greater systolic dysfunction and a more severe cardiomyopathic phenotype than dnNRSF Tg mice. Collectively, our findings suggest that endogenous ANP/BNP protects the heart against the death and progression of pathological remodeling in a mouse model of dilated cardiomyopathy and sudden death.
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