Transcription factor EB (TFEB)-mediated autophagy protects bovine mammary epithelial cells against H2O2-induced oxidative damage in vitro

Journal of Animal Science and Biotechnology

Renxu Chang¹  Shengbin Luo²  Hongdou Jia²  Chuang Xu²  Chunhui Jiang²  Qiushi Xu²  Xudong Sun²  Yan Tang²  Zhihao Dong²  Juan J. Loor³  Yusheng Liang³ 

[1] College of Veterinary Medicine, Hunan Agricultural University, 410128, Changsha, China;Heilongjiang Provincial Key Laboratory of Prevention and Control of Bovine Diseases, College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, No. 5 Xinyang Road, 163319, Daqing, Heilongjiang Province, China;Mammalian NutriPhysioGenomics, Department of Animal Sciences and Division of Nutritional Sciences, University of Illinois, 61801, Urbana, USA;

关键词: Apoptosis;    Autophagy;    Bovine mammary epithelial cells;    Oxidative stress;    TFEB;   

DOI  :  10.1186/s40104-021-00561-7

来源: Springer

【 摘 要 】

BackgroundBovine mammary epithelial cells after calving undergo serious metabolic challenges and oxidative stress both of which could compromise autophagy. Transcription factor EB (TFEB)-mediated autophagy is an important cytoprotective mechanism against oxidative stress. However, effects of TFEB-mediated autophagy on the oxidative stress of bovine mammary epithelial cells remain unknown. Therefore, the main aim of the study was to investigate the role of TFEB-mediated autophagy in bovine mammary epithelial cells experiencing oxidative stress.ResultsH2O2 challenge of the bovine mammary epithelial cell MAC-T increased protein abundance of LC3-II, increased number of autophagosomes and autolysosomes while decreased protein abundance of p62. Inhibition of autophagy via bafilomycin A1 aggravated H2O2-induced reactive oxygen species (ROS) accumulation and apoptosis in MAC-T cells. Furthermore, H2O2 treatment triggered the translocation of TFEB into the nucleus. Knockdown of TFEB by siRNA reversed the effect of H2O2 on protein abundance of LC3-II and p62 as well as the number of autophagosomes and autolysosomes. Overexpression of TFEB activated autophagy and attenuated H2O2-induced ROS accumulation. Furthermore, TFEB overexpression attenuated H2O2-induced apoptosis by downregulating the caspase apoptotic pathway.ConclusionsOur results indicate that activation of TFEB mediated autophagy alleviates H2O2-induced oxidative damage by reducing ROS accumulation and inhibiting caspase-dependent apoptosis.

【 授权许可】

CC BY