Differential effects of insulin-like growth factors on scratch wound repair in respiratory epithelial cells

Insulin-like growth factors (IGFs) I and II, being potent promoters of cellular growth and differentiation, were investigated for their effectiveness in improving the rate of scratch closure in human respiratory epithelium in vitro. Human epithelial cell lines from the nasal, bronchial, and tracheal...

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Veröffentlicht in:American journal of rhinology 2006-11, Vol.20 (6), p.652-657
Hauptverfasser: Adams, Damian H, McIntosh, David, Wormald, Peter-John, Cowin, Allison J
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Sprache:eng
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Zusammenfassung:Insulin-like growth factors (IGFs) I and II, being potent promoters of cellular growth and differentiation, were investigated for their effectiveness in improving the rate of scratch closure in human respiratory epithelium in vitro. Human epithelial cell lines from the nasal, bronchial, and tracheal regions were analyzed for their response to IGF-I and IGF-II, in a confluent monolayer scratch assay. IGF-binding proteins (IGFBPs) produced by certain cells are able to reduce the effectiveness of the IGFs. Consequently, the analogues LongR3 IGF-I, Des1-3 IGF-I and Arg3 IGF-I were investigated also because of their lower affinity for the IGFBPs, while still retaining unaffected affinity for the IGF-I receptor. All growth factors that were analyzed significantly improved the rate of scratch closure in bronchial and tracheal epithelial cells (p < or = 0.05). In comparison, scratch closure was markedly slower in nasal epithelial cells and IGF-I was the most effective growth factor at effecting scratch closure in these cells. The IGF-I analogues did not significantly improve scratch closure compared with IGF-I, despite the presence of IGFBP-3 in nasal, bronchial, and tracheal epithelial cells. Addition of IGF-I to wounded nasal epithelial cells increases the rate of scratch closure and therefore may have potential for improving the healing of the nasal mucosa.
ISSN:1050-6586
1945-8924
1539-6290
1945-8932
DOI:10.2500/ajr.2006.20.2916