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Research Article Free access | 10.1172/JCI115578

Autocrine angiotensin system regulation of bovine aortic endothelial cell migration and plasminogen activator involves modulation of proto-oncogene pp60c-src expression.

L Bell, D J Luthringer, J A Madri, and S L Warren

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Bell, L. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Luthringer, D. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

Find articles by Madri, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.

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

Published January 1, 1992 - More info

Published in Volume 89, Issue 1 on January 1, 1992
J Clin Invest. 1992;89(1):315–320. https://doi.org/10.1172/JCI115578.
© 1992 The American Society for Clinical Investigation
Published January 1, 1992 - Version history
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Abstract

Rapid endothelial cell migration and inhibition of thrombosis are critical for the resolution of denudation injuries to the vessel wall. Inhibition of the endothelial cell autocrine angiotensin system, with either the angiotensin-converting enzyme inhibitor lisinopril or the angiotensin II receptor antagonist sar1, ile8-angiotensin II, leads to increased endothelial cell migration and urokinase-like plasminogen activator (u-PA) activity (Bell, L., and J. A. Madri. 1990. Am. J. Pathol. 137:7-12). Inhibition of the autocrine angiotensin system with the converting-enzyme inhibitor or the receptor antagonist also leads to increased expression of the proto-oncogene c-src: pp60c-src mRNA increased 7-11-fold, c-src protein 3-fold, and c-src kinase activity 2-3-fold. Endothelial cell expression of c-src was constitutively elevated after stable infection with a retroviral vector containing the c-src coding sequence. Constitutively increased c-src kinase activity reconstituted the increases in migration and u-PA observed with angiotensin system interruption. Antisera to bovine u-PA blocked the increase in migration associated with increased c-src expression. These data suggest that increases in endothelial cell migration and plasminogen activator after angiotensin system inhibition are at least partially pp60c-src mediated. Elevated c-src expression with angiotensin system inhibition may act to enhance intimal wound closure and to reduce luminal thrombogenicity in vivo.

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