IGF-1 Promotes Endocytosis of Alveolar Epithelial Cells through PI3K Signaling

Abstract

Airway inflammation can be mitigated when apoptotic cells are engulfed by pulmonary epithelial cells. Insulin-like growth factor 1 (IGF-1), a single chain polypeptide growth factor, is the main mediator of growth hormone activity in vivo. IGF-1 has many biological activities, such as the regulation of cell survival, proliferation, differentiation and metabolism. However, its effect on the engulfment of cells, especially by non-professional phagocytes such as alveolar epithelial cells (AECs), has not been fully elucidated. We report that IGF-1 increases endocytosis in a mouse alveolar epithelial cell line, MLE-12. The PI3K-Akt pathway is involved in this effect of IGF-1. Furthermore, IGF-1 can inhibit the production of interleukin-6 in lipopolysaccharide-stimulated AECs. We have found that IGF-1 can enhance endocytosis of AECs through the PI3K pathway and exhibit anti-inflammatory properties. These two observations suggest that IGF-1 is a potential mediator in the regulation of airway inflammation.

Keywords: IGF-1; PI3K-Akt pathway; alveolar epithelial cells; endocytosis.