Expression of IGF-1, IGF-1 receptor and TGF-β following balloon angioplasty in atherosclerotic and normal rabbit iliac arteries: An immunocytochemical study

Maria B. Grant, Thomas J. Wargovich, David M. Bush, Denifield W. Player, Sergio Caballero, Marie Foegh, Polyxenie E. Spoerri

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

Growth factors have been implicated in the pathogenesis of restenosis (myointimal hyperplasia after coronary interventions). In this study, we examined the expression of insulin-like growth factor-I (IGF-1), IGF-1 receptor, and transforming growth factor-β (TGF-β) in atherosclerotic and normal rabbit iliac arteries following overstretch balloon angioplasty of the iliac arteries to create a vascular lesion. Animals were sacrificed at 0, 3, 7, 15 and 42 days post angioplasty. The iliac arteries were processed for immunocytochemical localization of IGF-1, IGF-1 receptor and TGF-β using colloidal gold and the data were quantitatively analyzed. IGF-1, IGF-1 receptor and TGF-β immunoreactivity were all significantly increased in atherosclerotic arteries compared to control at all of the time points examined. Following balloon angioplasty, the levels of IGF-1 and IGF-1 receptor increased significantly in both control and even further in hypercholesterolemic vessels. In control vessels, the IGF-1 levels returned to preintervention levels, while in atherosclerotic vessels, the levels of IGF-1 and IGF-1 receptor remained elevated. In addition, TGF-β levels in control vessels showed an initial rise in the first week following injury but then returned to baseline levels. In contrast, atherosclerotic vessels demonstrated a sustained expression of TGF-β. Thus, IGF-1 and TGF-β expression is different in normal vs. atherosclerotic vessels following vascular injury. The intensity of expression of IGF-1 and its receptor, which is not reduced at 42 days compared to 15 days following injury, support a role for IGF-1 in smooth muscle cell proliferation and migration. The sustained increase in TGF-β could facilitate extracellular matrix (ECM) accumulation. Local vascular therapy that is directed towards modulating the effects of IGF-1 and TGF-β could reduce restenosis. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)47-53
Number of pages7
JournalRegulatory Peptides
Volume79
Issue number1
DOIs
StatePublished - Jan 1 1999

Keywords

  • Atherosclerosis
  • Growth factors
  • Myointimal hyperplasia
  • Restenosis

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

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