IGF-I, EGF, and sex steroids regulate autophagy in bovine mammary epithelial cells via the mTOR pathway

摘要: Mammary gland growth and involution are based on a dynamic equilibrium between proliferation apoptosis of mammary epithelial cells (MEC). The main type cell death responsible for bovine is apoptosis, but MEC also exhibit morphological features autophagy. present study has been undertaken in order to examine factors, which the regulation autophagy MEC. We used model vitro known be dependent fetal serum (FBS) deficiency culture BME-UV1 cells. investigated effects insulin-like factor-1 (IGF-I) epidermal factor (EGF) signaling, as well sex steroids rapamycin (a specific inhibitor mammalian target rapamycin, mTOR, kinase) line BME-UV1. Our focus was role mTOR by factors hormones. Laser scanning cytometry, electron microscopy, Western-blot analysis, GFP-LC3 reporter-based expression LysoTracker Green-related fluorescence were determine activity found that FBS induced both with highest intensity processes after 48h exposure deficient medium (0.5% FBS). Addition IGF-I or/and EGF FBS-deficient clearly diminished show involved activation MEC, whereas inhibition abrogated suppressive This suggests links signaling inhibiting pathways. Contrary EGF, 17beta-estradiol progesterone exerted stimulatory At same time we observed effect activation/phosphorylation. In conclusion, undergoes complex regulation, where its controlled survival pathways suppression autophagy, pregnancy steroids, act inducers process.