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ERK1/2-mediated autophagy is essential for cell survival under Ochratoxin A exposure in IPEC-J2 cells

Hong Wang1, Hu Li1, Xingxiang Chen1

  • 1College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province 210095, China; Institute of Nutritional and Metabolic Disorders in Domestic Animals and Fowls, Nanjing Agricultural University, Nanjing, Jiangsu Province 210095, China.

Toxicology and Applied Pharmacology
|September 25, 2018
PubMed

Insights

Porcine intestinal epithelial cells utilize ERK1/2-mediated autophagy to survive Ochratoxin A (OTA) toxicity. Inhibiting this pathway exacerbates OTA-induced cell death, highlighting a crucial protective mechanism against mycotoxin contamination.

Area of Science:

  • * Gastroenterology and Toxicology
  • * Cellular and Molecular Biology

Background:

  • * The intestinal epithelium is a primary defense against foodborne contaminants like Ochratoxin A (OTA), a prevalent mycotoxin.
  • * Understanding cellular defense mechanisms against OTA is crucial for food safety and animal health.

Purpose of the Study:

  • * To investigate the adaptive cytoprotective mechanisms of intestinal epithelial cells against OTA exposure.
  • * To elucidate the regulatory pathways involved in cellular defense against OTA.

Main Methods:

  • * Utilized the intestinal porcine epithelial cell line (IPEC-J2) as an in vitro model.
  • * Employed Western blot, immunofluorescence, Hoechst 33258 staining, and Annexin V/PI analysis.
  • * Investigated the roles of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and autophagy using specific inhibitors (U0126 and Chloroquine).

Main Results:

  • * OTA induced ERK1/2 activation and autophagy in IPEC-J2 cells.
  • * Inhibition of ERK1/2 (U0126) aggravated OTA-induced apoptosis.
  • * Inhibition of autophagy (Chloroquine) enhanced OTA-induced apoptosis, mitochondrial damage, and caspase-3 activation.

Conclusions:

  • * ERK1/2-mediated autophagy is essential for the survival of porcine intestinal epithelial cells exposed to OTA.
  • * This pathway represents a critical adaptive response to mitigate OTA toxicity in the gut.
Keywords:
ApoptosisAutophagyExtracellular signal-regulated protein kinases 1 and 2IPEC-J2 cellsMitochondrial reactive oxygen speciesOchratoxin A

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