TY - JOUR
T1 - Insulin-like growth factor-I and type I insulin-like growth factor receptor in 85% O2-exposed rat lung
AU - Han, Robin N.N.
AU - Han, Victor K.M.
AU - Buch, Shilpa
AU - Freeman, Bruce A.
AU - Post, Martin
AU - Keith Tanswell, A.
PY - 1996
Y1 - 1996
N2 - 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.
AB - 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.
KW - Airway hyperreactivity
KW - Cell interactions
KW - Lung injury
KW - Pulmonary hypertension
KW - Pulmonary oxygen toxicity
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M3 - Article
AN - SCOPUS:33745330812
SN - 0002-9513
VL - 271
SP - L150-L158
JO - American Journal of Physiology
JF - American Journal of Physiology
IS - 1 PART 1
ER -