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- Title
Transcription factor EB (TFEB)-mediated autophagy protects bovine mammary epithelial cells against H2O2-induced oxidative damage in vitro.
- Authors
Sun, Xudong; Chang, Renxu; Tang, Yan; Luo, Shengbin; Jiang, Chunhui; Jia, Hongdou; Xu, Qiushi; Dong, Zhihao; Liang, Yusheng; Loor, Juan J.; Xu, Chuang
- Abstract
Background: Bovine 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. Results: H2O2 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. Conclusions: Our results indicate that activation of TFEB mediated autophagy alleviates H2O2-induced oxidative damage by reducing ROS accumulation and inhibiting caspase-dependent apoptosis.
- Subjects
EPITHELIAL cells; TRANSCRIPTION factors; BOS; REACTIVE oxygen species; OXIDATIVE stress; AUTOPHAGY
- Publication
Journal of Animal Science & Biotechnology, 2021, Vol 12, Issue 1, p1
- ISSN
1674-9782
- Publication type
Article
- DOI
10.1186/s40104-021-00561-7