ROS activates autophagy in follicular granulosa cells via mTOR pathway to regulate broodiness in goose

Abstract

Broodiness causes reduced reproductive ability in poultry, but its regulatory mechanism remains poorly understood. ROS (reactive oxygen species) and autophagy are important for follicular development, and the interaction between the two may play a role in regulating broodiness. We examined goose follicles for ROS and oxidation scavenger activities during the egg-laying and broody stages. The follicular granulosa cells were exposed to media containing H₂O₂, and the interactions between ROS and autophagy in follicular granulosa cells in vitro were analyzed using a Western blot method. We found that the activities of superoxide dismutase (SOD) and lactate dehydrogenase (LDH) were enhanced and the amount of malondialdehyde (MDA) decreased in broody goose follicles. H₂O₂ inhibited the cell viability and induced autophagy. Furthermore, it was also found that H₂O₂ regulated autophagy by reducing mTOR and increasing p53; however, H₂O₂ had no impact on Beclin1 or ATG12. It was also shown that the enhanced autophagy lessened ROS-induced damages. We conclude that ROS and autophagy both played important roles in regulating follicular development to control broodiness in geese, and ROS activated autophagy in follicular granulosa cells via the mTOR pathway.

Keywords: Autophagy; Broodiness; Granulosa cell; ROS; mTOR.