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Research Article Free access | 10.1172/JCI117669

Localization of heparin-binding EGF-like growth factor in the smooth muscle cells and macrophages of human atherosclerotic plaques.

J Miyagawa, S Higashiyama, S Kawata, Y Inui, S Tamura, K Yamamoto, M Nishida, T Nakamura, S Yamashita, and Y Matsuzawa

Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Second Department of Internal Medicine, Osaka University Medical School, Yamadaoka, Japan.

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Published January 1, 1995 - More info

Published in Volume 95, Issue 1 on January 1, 1995
J Clin Invest. 1995;95(1):404–411. https://doi.org/10.1172/JCI117669.
© 1995 The American Society for Clinical Investigation
Published January 1, 1995 - Version history
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Abstract

Heparin-binding EGF-like growth factor (HB-EGF) is a potent chemoattractant and mitogen for smooth muscle cells (SMC) in culture. To elucidate whether HB-EGF is implicated in the pathogenesis of human atherosclerosis, we examined immunohistochemical localization of HB-EGF in human aortic walls and atherosclerotic plaques. The medial SMC of the aorta in babies and children synthesized HB-EGF protein, while the number of SMC producing HB-EGF was dramatically decreased in young and middle-aged adults. In atherosclerotic plaques, however, marked production of HB-EGF protein was detected in SMC and macrophages of the plaques. Furthermore, EGF receptors, to which HB-EGF is known to bind, were detected in plaque SMC. These data suggest that HB-EGF may be implicated in the migration and proliferation of SMC that occurs in the normal development of arterial walls, and in the formation of atherosclerotic plaques.

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