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

4 Scopus citations

Abstract

The expression of insulin-like growth factor I(IGF-I) and insulinlike 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) was assessed by immunohistochemistry. IGF-I, but not IGF-II, was localized to airway epithelium, while IGF-IK was localized to perivascular and peribronchial cells, in the lungs of animals breathing air. IGF-II mRNA did not increase with exposure to 85% 0%, 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 eridothelial 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)L150-L158
JournalAmerican Journal of Physiology
Volume271
Issue number1 PART 1
StatePublished - 1996
Externally publishedYes

Keywords

  • Airway hyperreactivity
  • Cell interactions
  • Lung injury
  • Pulmonary hypertension
  • Pulmonary oxygen toxicity

ASJC Scopus subject areas

  • Physiology (medical)

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