Upregulation of IGF-I and collagen I mRNA in human atherosclerotic tissue is not accompanied by changes in type 1 IGF receptor or collagen III mRNA: an in situ hybridization study

V J Wilson, J P Ward, K G Burnand, C R Thomas

Research output: Contribution to journalArticle (Academic Journal)peer-review

13 Citations (Scopus)

Abstract

BACKGROUND: Immunoreactive insulin-like growth factor-I (IGF-I) has recently been localized to vascular smooth muscle cells in coronary atherectomy plaques, but it remains unclear whether these cells are the source of this growth factor. We therefore investigated the gene expression of this factor, and the expression of the genes for its receptor and two types of collagen known to be regulated by IGF-I, in vascular tissue samples from patients with atherosclerosis or restenosis.

METHODS: Gene expression and localization were investigated by in situ hybridization, using 35S-labelled complementary RNA probes specific for IGF-I, its type a receptor, collagen I, and collagen III. The cellular composition of the tissue samples was determined by immunohistochemistry using antibodies specific for smooth muscle cells and macrophages.

RESULTS: IGF-I and collagen I messenger RNAs were found in areas containing smooth muscle cells and macrophages, but collagen III and type 1 IGF receptor gene expression could not be detected in any tissue samples.

CONCLUSION: IGF-I appears to be involved in the progression of the atherosclerotic plaque, even at an advanced stage, but preliminary data from two restenotic plaques indicate that it may not be involved in the later stages of restenosis.

Original languageEnglish
Pages (from-to)569-72
Number of pages4
JournalCoronary Artery Disease
Volume7
Issue number8
Publication statusPublished - Aug 1996

Keywords

  • Arteriosclerosis
  • Culture Techniques
  • Gene Expression
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization
  • Insulin-Like Growth Factor I
  • Integrins
  • RNA, Messenger
  • Receptors, Collagen
  • Journal Article
  • Research Support, Non-U.S. Gov't

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