[IGF-1 activates the PI3K pathway through S1P/S1PR1 signaling to promote the migration of mouse alveolar epithelial cells].

Objective To investigate the effect of insulin-like growth factor 1 (IGF-1) on the migration of alveolar epithelial cells (AECs) and its related mechanisms. Methods The MLE-12 cells (mouse AEC line) were stimulated by IGF-1 and sphingosine 1 phosphate (S1P) in the presence or absence of the PI3K inhibitor Wortmannin. Then, the cell migration was detected by the scratch test and the expression of p-Akt was detected by Western blot. With AECs stimulated by IGF-1, the secretion and expression of S1P were tested by ELISA and Western blot respectively. In the blocking experiment, the effect of IGF-1 on cell migration or p-Akt expression was detected by scratch test or Western blot after the interference of AEC S1P receptor 1 (S1PR1) or the action of S1PR1 blocking antibody. Results After 12 hours of IGF-1 stimulation, the expression of p-Akt in AECs increased and the migration of AECs accelerated. When blocking PI3K signal, the effect of IGF-1 on promoting AEC migration was partially eliminated. IGF-1 induced AECs to produce S1P, which accelerated AEC migration through S1PR1. The expression of p-Akt in AECs increased after S1P stimulation. When blocking the PI3K pathway, the ability of S1P to accelerate the migration of AECs was reduced. When S1PR1 in AECs was blocked or interfered, the effect of IGF-1 on accelerating AEC migration and promoting AEC p-Akt expression was partially reduced. Conclusion IGF-1 activates the PI3K pathway through S1P-S1PR1 signal to promote the migration of AECs.