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

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 func...

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Autores principales:	Lu Liu, Manjiang Wang, Ning Gong, Peng Tian, Hongxia Deng
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	ferroptosis selenium heat stress gpx4 sod Medicine (General) R5-920 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/a2d8aec510404cf689188e8ce059ef18
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spelling	oai:doaj.org-article:a2d8aec510404cf689188e8ce059ef182021-11-04T15:00:42ZSe improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells1976-83542151-248510.1080/19768354.2021.1988704https://doaj.org/article/a2d8aec510404cf689188e8ce059ef182021-09-01T00:00:00Zhttp://dx.doi.org/10.1080/19768354.2021.1988704https://doaj.org/toc/1976-8354https://doaj.org/toc/2151-2485Selenium (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.Lu LiuManjiang WangNing GongPeng TianHongxia DengTaylor & Francis Grouparticleferroptosisseleniumheat stressgpx4sodMedicine (General)R5-920Biology (General)QH301-705.5ENAnimal Cells and Systems, Vol 25, Iss 5, Pp 283-295 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	ferroptosis selenium heat stress gpx4 sod Medicine (General) R5-920 Biology (General) QH301-705.5
spellingShingle	ferroptosis selenium heat stress gpx4 sod Medicine (General) R5-920 Biology (General) QH301-705.5 Lu Liu Manjiang Wang Ning Gong Peng Tian Hongxia Deng Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
description	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.
format	article
author	Lu Liu Manjiang Wang Ning Gong Peng Tian Hongxia Deng
author_facet	Lu Liu Manjiang Wang Ning Gong Peng Tian Hongxia Deng
author_sort	Lu Liu
title	Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
title_short	Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
title_full	Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
title_fullStr	Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
title_full_unstemmed	Se improves GPX4 expression and SOD activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
title_sort	se improves gpx4 expression and sod activity to alleviate heat-stress-induced ferroptosis-like death in goat mammary epithelial cells
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/a2d8aec510404cf689188e8ce059ef18
work_keys_str_mv	AT luliu seimprovesgpx4expressionandsodactivitytoalleviateheatstressinducedferroptosislikedeathingoatmammaryepithelialcells AT manjiangwang seimprovesgpx4expressionandsodactivitytoalleviateheatstressinducedferroptosislikedeathingoatmammaryepithelialcells AT ninggong seimprovesgpx4expressionandsodactivitytoalleviateheatstressinducedferroptosislikedeathingoatmammaryepithelialcells AT pengtian seimprovesgpx4expressionandsodactivitytoalleviateheatstressinducedferroptosislikedeathingoatmammaryepithelialcells AT hongxiadeng seimprovesgpx4expressionandsodactivitytoalleviateheatstressinducedferroptosislikedeathingoatmammaryepithelialcells
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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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