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Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells

ABSTRACT: ABSTRACT Selenium (Se) is a vital element of life, which has an important impact on the growth, development, production performance and stress-tolerance of animals. However, it is not entirely clear that how exactly Se works during these processes. Herein, we investigate the role of Se in regulating the functions of goat mammary epithelial cells (GMECs) under heat-stress condition. We found that heat stress caused ferroptosis-like death in GMECs, manifested by a robust increase in iron ion concentration, reactive oxygen species (ROS) and cell death ratio, and a decrease in the activity of superoxide dismutase (SOD) and expression level of glutathione peroxidases 4 (GPX4). Se incubation had no obvious effect on GMEC viability, but alleviated heat-stress-induced ferroptosis-like cell death and improved GPX4 expression and SOD activity in a dose-dependent manner. Also, we found that overexpression of GPX4 could improve the activity of SOD. And Se incubation inhibited activation of mTOR signaling in heat-stress-induced GMECs, which could be eliminated by the mTOR activator MHY1485, and treatment with mTOR inhibitor AY-22989 had the same effect as Se. In conclusion, Se improves GPX4 expression and SOD activity and inhibits the activation of mTOR to alleviate heat-stress-induced ferroptosis-like death in GMECs, which may be a protective agent for heat stress in goats.

SUBMITTER: Liu L

PROVIDER: S-EPMC8567913 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe notable decline in the number of Tregs within Necrotizing enterocolitis (NEC) intestinal tissues，contribute to excessive inflammation and necrosis, yet the precise underlying factors remain enigmatic. Ferroptosis, a novel cell death stemming from a disrupted lipid redox metabolism, is the focus of this investigation. Specifically, this study delves into the ferroptosis of Treg cells in the context of NEC and observes the protective effects exerted by vitamin E intervention, which aims to mitigate ferroptosis of Treg cells.MethodsTo investigate the reduction of Treg cells in NEC intestine, we analyzed its association with ferroptosis from multiple angles. We constructed a mouse with a specific knockout of Gpx4 in Treg cells, aiming to examine the impact of Treg cell ferroptosis on NEC intestinal injury and localized inflammation. Ultimately, we employed vitamin E treatment to mitigate ferroptosis in NEC intestine's Treg cells, monitoring the subsequent amelioration in intestinal inflammatory damage.ResultsThe diminution of Treg cells in NEC is attributed to ferroptosis stemming from diminished GPX4 expression. Gpx4-deficient Treg cells exhibit impaired immunosuppressive function and are susceptible to ferroptosis. This ferroptosis of Treg cells exacerbates intestinal damage and inflammatory response in NEC. Notably, Vitamin E can inhibit the ferroptosis of Treg cells, subsequently alleviating intestinal damage and inflammation in NEC. Additionally, Vitamin E bolsters the anti-lipid peroxidation capability of Treg cells by upregulating the expression of GPX4.ConclusionIn the context of NEC, the ferroptosis of Treg cells represents a significant factor contributing to intestinal tissue damage and an exaggerated inflammatory response. GPX4 is pivotal for the viability and functionality of Treg cells. Vitamin E exhibits the capability to mitigate the ferroptosis of Treg cells, thereby enhancing their number and function, which plays a crucial role in mitigating intestinal tissue damage and inflammatory response in NEC.

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Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells

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