Oxyresveratrol Induces Autophagy via the ER Stress Signaling Pathway, and Oxyresveratrol-Induced Autophagy Stimulates MUC2 Synthesis in Human Goblet Cells.

Jiah Yeom,Young-Hee Lim,Seongho Ma

doi:10.3390/antiox9030214

Jiah Yeom, Young-Hee Lim + Show 1 more

Open Access

https://doi.org/10.3390/antiox9030214

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Journal: Antioxidants	Publication Date: Mar 5, 2020
Citations: 6	License type: CC BY 4.0

Affiliation: Korea University, Korea University Medical Center

Abstract

Background: Autophagy is a cell protection system invoked to eliminate the damaged organelles and misfolded proteins that induce various stresses, including endoplasmic reticulum (ER) stress. Autophagy can control mucin secretion in goblet cells. Oxyresveratrol (OXY), an antioxidant, stimulates expression of MUC2. Thus, we investigated the effect of OXY on autophagy and found that OXY-induced autophagy stimulates MUC2 expression in human intestinal goblet cells. Methods: Autophagy-related genes and proteins were examined by quantitative real-time PCR (qPCR) and Western blotting, respectively. Autophagy was assessed by immunocytochemistry (ICC). To analyze the protein expression profiles of OXY-treated LS 174T goblet cells, two-dimensional electrophoresis (2DE) and peptide mass fingerprinting (PMF) were performed. MUC2 expression in cells was evaluated by ICC. Results: OXY significantly increased the expression levels of genes related to autophagy induction, and activated phagosome elongation resulted in the formation of autophagosomes. OXY also activated the ER stress signaling pathway and promoted MUC2 synthesis, which was inhibited by treatment with an autophagy inhibitor. Conclusion: OXY induces autophagy via the ER stress signaling pathway, and OXY-induced autophagy increases MUC2 production in intestinal goblet cells.

Highlights

Autophagy is a self-digesting process that is characterized by the removal of damaged organelles, misfolded proteins, and old or nonfunctional proteins [1,2]
The results suggest that Atg5, which forms a complex with other Atg proteins and participates in autophagosome membrane elongation, is stimulated through MEK/ERK signaling induced by OXY treatment but that LC3B, which accounts for the major complex of doublemembraned autophagosomes and is most widely used as an autophagy marker, is not associated
The results suggest that OXY-dependent Beclin-1, Atg7, and Atg5 stimulation may partially occur via the MEK/ERK signaling pathway but that OXY-induced autophagy might not be regulated by Mitogen-Activated Protein Kinase (MAPK) kinase

Summary

Introduction

Autophagy is a self-digesting process that is characterized by the removal of damaged organelles, misfolded proteins, and old or nonfunctional proteins [1,2]. This system is a type of survival mechanism that is triggered in response to diverse stresses, such as starvation and hypoxia, to maintain intracellular homeostasis. Autophagy is a cell protection system invoked to eliminate the damaged organelles and misfolded proteins that induce various stresses, including endoplasmic reticulum (ER). We investigated the effect of OXY on autophagy and found that OXY-induced autophagy stimulates MUC2 expression in human intestinal goblet cells

Methods

Results

Conclusion