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Research Article Free access | 10.1172/JCI116460

Protamine and protamine-insulins exacerbate the vascular response to injury.

E R Edelman, L A Pukac, and M J Karnovsky

Department of Internal Medicine, Brigham and Women's Hospital, Boston, Massachusetts.

Find articles by Edelman, E. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Brigham and Women's Hospital, Boston, Massachusetts.

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

Department of Internal Medicine, Brigham and Women's Hospital, Boston, Massachusetts.

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

Published May 1, 1993 - More info

Published in Volume 91, Issue 5 on May 1, 1993
J Clin Invest. 1993;91(5):2308–2313. https://doi.org/10.1172/JCI116460.
© 1993 The American Society for Clinical Investigation
Published May 1, 1993 - Version history
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Abstract

Endothelial cells and smooth muscle cells produce heparinlike compounds that are growth inhibitory for vascular smooth muscle cells, and it has been suggested that these compounds play a regulatory role that is perturbed with vascular injury. Indeed, exogenous heparin preparations effectively suppress smooth muscle cell proliferation following injury imposed on vascular endothelium. We now report that protamine, an agent that binds heparin and negates its anticoagulant properties, has potent stimulatory effects on vascular smooth muscle cell proliferation. The administration of protamine, alone or as part of commonly used insulin preparations, stimulated the proliferation of cultured smooth muscle cells, exacerbated vascular smooth muscle cell proliferative lesions in laboratory rats, and interfered with the growth-inhibitory effects of heparin in culture and in vivo. These results confirm the importance of endogenous heparinlike compounds in arterial homeostasis and may require reconsideration of protamine use following vascular reparative procedures and in diabetics.

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