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Department of Pathology and Laboratory Medicine (B.Z., D.Y.H.), Division of Endocrinology and Metabolism (G.Z., J.A.F.), University of Cincinnati, and Department of Pathology, Children’s Hospital Medical Center (D.P.W.), Cincinnati, Ohio 45267
Address all correspondence and requests for reprints to: James A. Fagin, M.D., Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Vontz Center for Molecular Studies, 3125 Eden Avenue, Cincinnati, Ohio 45267. E-mail: faginja{at}uc.edu
The response of arterial smooth muscle cells to injury is governed
by a complex series of events. Significant among them is the paracrine
production of peptide growth factors. To determine the impact of local
IGF-I gene expression on vascular injury, the left carotid arteries of
SMP8-IGF-I mice (in which IGF-I is selectively overexpressed in smooth
muscle cells by means of a smooth muscle 
-actin promoter) and
wild-type controls were injured mechanically with an epon resin probe.
After 7 and 14 d, a progressive increase in medial area was seen
in both SMP8-IGF-I and wild-type mice, but they were not significantly
different from each other. However, by 14 d there was a more than
4-fold increase in neointimal area in transgenic vs.
wild-type. The intima/media ratios were also strikingly increased at
14 d in the IGF-I-overexpressing animals. The mitotic index,
determined in animals injected daily with bromodeoxyuridine for 3
d before death, was markedly elevated in both the media and neointima
7 d after injury in SMP8-IGF-I mice, but the effect had subsided
by 14 d. Despite a higher rate of cell division, the relative
increase in medial area was less in the SMP8-IGF-I mice than in
wild-type mice at both 7 and 14 d, consistent with a stimulation
of cell migration to the neointima. The experiments reported here
provide compelling evidence that paracrine expression of IGF-I is a
powerful stimulus for smooth muscle cell proliferation and migration
in vivo.
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