The role of autophagy in intestinal epithelial injury
link.springer.com shows its articles on its own site.
Read the article on link.springer.com ↗Article · Sep 2019 · 1 min read
In brief
In brief
This study investigates autophagy regulation in intestinal epithelial cells during injury induced by hypoxia and LPS. Findings demonstrate that excessive autophagosome accumulation is detrimental to cell survival, while inhibiting autophagy initiation improves viability, suggesting therapeutic potential for intestinal injury conditions.
Written by the GCMD Library team from the article.
Abstract
Purpose
Autophagy is a natural mechanism aimed to degrade and recycle cellular components within cells. Previous studies reported that autophagy in the intestinal epithelium can be activated and that excessive autophagy can have negative consequences. However, the mechanism by which autophagy is regulated during intestinal epithelial injury remains unclear. This study aimed to investigate the mechanism of autophagy regulation during intestinal epithelial cells (IEC) injury.
Methods
Rat IEC18 were exposed to hypoxia and Lipopolysaccharide (LPS) (200 μg/ml) to induce injury. IEC18 were treated with autophagy initiation inhibitor, Wortmannin or with autophagy degradation inhibitor, Bafilomycin A1 were added for 24 h. We assessed the number and diameter of autophagic vacuoles, Cell viability, inflammation and apoptosis.
Results
Hypoxia and LPS administration increased the number and diameter of autophagic vacuoles in IEC18. Wortmannin administration reduced the number and diameter of autophagic vacuoles. On the contrary, Bafilomycin A1 administration increased the number of autophagic vacuoles. Cell viability increased following administration of Wortmannin and decreased following administration of Bafilomycin A1.
Conclusions
We found that accumulation of autophagic vacuoles which characterize excessive or incomplete autophagy was detrimental to cell survival. This was shown by an increase in the number and size of the autophagic vacuoles with Bafilomycin A1treatment after hypoxia and LPS stressors relative to hypoxia and LPS alone. Conversely, there was a decrease in the number of autophagic vacuoles with Wortmannin treatment after hypoxia and LPS stressors relative to hypoxia and LPS alone. Therefore, reducing autophagosomes accumulation may represent a novel therapeutic strategy for intestinal injury.