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Research Article Free access | 10.1172/JCI118660

Neutral endopeptidase 24.11 in neutrophils modulates protective effects of natriuretic peptides against neutrophils-induced endothelial cytotoxity.

T Matsumura, K Kugiyama, S Sugiyama, M Ohgushi, K Amanaka, M Suzuki, and H Yasue

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Matsumura, T. in: PubMed | Google Scholar

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Kugiyama, K. in: PubMed | Google Scholar

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Sugiyama, S. in: PubMed | Google Scholar

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Ohgushi, M. in: PubMed | Google Scholar

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Amanaka, K. in: PubMed | Google Scholar

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Suzuki, M. in: PubMed | Google Scholar

Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.

Find articles by Yasue, H. in: PubMed | Google Scholar

Published May 15, 1996 - More info

Published in Volume 97, Issue 10 on May 15, 1996
J Clin Invest. 1996;97(10):2192–2203. https://doi.org/10.1172/JCI118660.
© 1996 The American Society for Clinical Investigation
Published May 15, 1996 - Version history
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Abstract

This study was performed to determine effects of atrial and brain natriuretic peptides (ANP, BNP) on neutrophils-induced endothelial injury which is known to play a role in the pathophysiology of ischemia/reperfusion myocardial injury and to examine whether the effects of ANP and BNP on neutrophils are modulated by neutral endopeptidase 24.11 (NEP) in neutrophils themselves. The incubation of human neutrophils with ANP and BNP inhibited the neutrophils-induced detachment of cultured human endothelial cells (HEC). The inhibitory effect of ANP and BNP was associated with the suppressions of the neutrophils adhesiveness to HEC, CD18 expression on the neutrophils and elastase release from the neutrophils. Coincubation with UK73967 or phosphoramidon, inhibitors of NEP, potentiated all of the effects of ANP and BNP on the neutrophil functions, and the NEP inhibitors protected degradation of ANP and BNP by the neutrophils. NEP enzymatic activity in the particulate fractions and immunoreactive NEP expression were found to increase in the neutrophils from patients with early phase of acute myocardial infarction (AMI) by 5.2- and by 4.2-fold of the neutrophils from patients with late phase of AMI, respectively. In an in vivo canine model of myocardial ischemia/reperfusion, the intravenous administration of UK73967 suppressed the neutrophil adherence to endothelium and the neutrophil accumulation in the ischemic/reperfused myocardium. The results indicate that ANP and BNP, which are known to increase in AMI, modulate the neutrophil functions and exert protective effects against the neutrophils-induced endothelial cytotoxity. But the effects are suppressed due to their degradation by the neutrophil own NEP. Thus, neutrophil NEP, which also increases in AMI, may play a role in the pathophysiology of neutrophils-mediated ischemia/reperfusion endothelial and myocardial injury.

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