Insulin-like growth factor-I and type I insulin-like growth factor receptor in 85% O2-exposed rat lung

Robin N.N. Han, Victor K.M. Han, Shilpa Buch, Bruce A. Freeman, Martin Post, A. Keith Tanswell

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

The expression of insulin-like growth factor I (IGF-I) and insulin- like growth factor II (IGF-II) was studied in the lungs of adult rats exposed to air or 85% O2, using Northern analysis, in situ hybridization, and immunohistochemistry. Distribution of the type I insulin-like growth factor receptor (IGF-IR) wa s assessed by immunohistochemistry. IGF-I, but not IGF-II, was localized to airway epithelium, while IGF-IR was localized to perivascular and peribronchial cells, in the lungs of animals breathing air. IGF-II mRNA did not increase with exposure to 85% O2, but IGF-II was localized to sites of perivascular edema and to occasional peribronchial cells. A widespread increase in IGF-I mRNA and peptide was seen after both a 6-day and a 14-day exposure to O2, with maximal expression in the airway and alveolar epithelium, and lesser expression in interstitial cells. After 6 days in 85% O2, increased IGF-IR immunoreactivity was localized to both perivascular and peribronchial cells and to endothelial cells. By 14 days in 85% O2, IGF-IR immunoreactivity was also localized to alveolar epithelial cells. The distribution of IGF-IR immunoreactivity was consistent with a paracrine role for IGF-I in O2-mediated pulmonary hypertension and airway hyperreactivity, by mediating smooth muscle cell hyperplasia, as well as a role in endothelial cell repair and late pneumocyte hyperplasia. The relative insensitivity of IGF-IR immunohistochemistry did not allow us to identify cells with low abundance IGF-IR, and potential cellular targets for IGF-I actions after O2-exposure may be even more extensive than those recognized here.

Original languageEnglish (US)
Pages (from-to)L139-L149
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume271
Issue number1 15-1
DOIs
StatePublished - 1996

Keywords

  • airway hyperreactivity
  • cell interactions
  • lung injury
  • pulmonary hypertension
  • pulmonary oxygen toxicity

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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