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mTORC1 signaling activation increases intestinal stem cell activity and promotes epithelial cell proliferation.

Authors
  • Zhou, Jia-Yi1
  • Huang, Deng-Gui1
  • Qin, Ying-Chao1
  • Li, Xiang-Guang2
  • Gao, Chun-Qi1
  • Yan, Hui-Chao1
  • Wang, Xiu-Qi1
  • 1 Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, China. , (China)
  • 2 Department of Pharmaceutical Engineering, School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China. , (China)
Type
Published Article
Journal
Journal of Cellular Physiology
Publisher
Wiley (John Wiley & Sons)
Publication Date
Aug 01, 2019
Volume
234
Issue
10
Pages
19028–19038
Identifiers
DOI: 10.1002/jcp.28542
PMID: 30937902
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The crypt-villus axis of the intestine undergoes a continuous renewal process that is driven by intestinal stem cells (ISCs). However, the homeostasis is disturbed under constant exposure to high ambient temperatures, and the precise mechanism is unclear. We found that both EdU+ and Ki67+ cell ratios were significantly reduced after exposure to 41°C, as well as the protein synthesis rate of IPEC-J2 cells, and the expression of ubiquitin and heat shock protein 60, 70, and 90 were significantly increased. Additionally, heat exposure decreased enteroid expansion and budding efficiency, as well as induced apoptosis after 48 hr; however, no significant difference was observed in the apoptosis ratio after 24 hr. In the process of heat exposure, the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway was significantly inhibited in both IPEC-J2 cells and enteroids. Correspondingly, treatment of IPEC-J2 and enteroids with the mTORC1 agonist MHY1485 at 41°C significantly attenuated the inhibition of proliferation and protein synthesis, increased the ISC activity, and promoted expansion and budding of enteroid. In summary, we conclude that the mTORC1 signaling pathway regulates intestinal epithelial cell and stem cell activity during heat exposure-induced injury. © 2019 Wiley Periodicals, Inc.

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