Endoplasmic reticulum stress-induced apoptosis in intestinal epithelial cells: A feed-back regulation by mechanistic target of rapamycin complex 1 (mTORC1)

20Citations
Citations of this article
22Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Background: Endoplasmic reticulum (ER) stress is associated with multiple pathological processes of intestinal diseases. Despite a critical role of mechanistic target of rapamycin complex 1 (mTORC1) in regulating cellular stress response, the crosstalk between mTORC1 and ER stress signaling and its contribution to the intestinal barrier function is unknown. Results: In the present study, we showed that intestinal epithelial cells (IEC-6) incubated with tunicamycin led to caspase-3-dependent apoptotic cell death. The induction of cell death was accompanied by activation of unfolded protein response as evidenced by increased protein levels for BiP, p-IRE1α, p-eIF2α, p-JNK, and CHOP. Further study demonstrated that tunicamycin-induced cell death was enhanced by rapamycin, a specific inhibitor of mTORC1. Consistently, tunicamycin decreased transepithelial electrical resistance (TEER) and increased permeability of the cells. These effects of tunicamycin were exacerbated by mTORC1 inhibitor. Conclusions: Taken together, the data presented here identified a previously unknown crosstalk between an unfold protein response and mTORC1 signaling in the intestinal epithelium. This feed-back loop regulation on ER stress signaling by mTORC1 is critical for cell survival and intestinal permeability in epithelial cells.

Cite

CITATION STYLE

APA

Ji, Y., Luo, X., Yang, Y., Dai, Z., Wu, G., & Wu, Z. (2018). Endoplasmic reticulum stress-induced apoptosis in intestinal epithelial cells: A feed-back regulation by mechanistic target of rapamycin complex 1 (mTORC1). Journal of Animal Science and Biotechnology, 9(1). https://doi.org/10.1186/s40104-018-0253-1

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free