IGF-1 Promotes Endocytosis of Alveolar Epithelial Cells through PI3K Signaling
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Updated: Jan 28, 2026

Flow Cytometric Isolation of Primary Murine Type II Alveolar Epithelial Cells for Functional and Molecular Studies
Published on: December 26, 2012
Helong Wang1, Jing He1, Yulan Luo1
1Department of Immunology, Anhui Provincial Key Laboratory of Infection and Immunity, Bengbu Medical College, Bengbu, Anhui, China.
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.
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