Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

Liqi Zhu1, Chunxiao Mou1, Xing Yang1

  • 1Key Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural University, Nanjing, Jiangsu, People's Republic of China.

Oncotarget
|March 31, 2016
PubMed

Insights

Transmissible gastroenteritis virus (TGEV) triggers mitophagy, a cellular process, in pigs to reduce oxidative stress and apoptosis. This mechanism may aid cell survival and viral infection.

Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Intestinal epithelial cells rely on mitochondria for absorption and barrier function.
  • Mitophagy is crucial for mitochondrial quality control and cellular homeostasis.
  • Transmissible gastroenteritis virus (TGEV) causes severe diarrhea in piglets, but its effect on mitophagy is unknown.

Purpose of the Study:

  • To investigate the role of mitophagy in TGEV infection of porcine epithelial cells.
  • To understand how TGEV impacts mitochondrial health and cellular responses.

Main Methods:

  • Infection of porcine epithelial cells (IPEC-J2) with TGEV.
  • Observation of mitochondrial morphology and mitophagy.
  • Analysis of oxidative stress markers and apoptosis.
  • Gene silencing of DJ-1 to assess its role.

Main Results:

  • TGEV infection induced mitochondrial injury and mitophagy in IPEC-J2 cells.
  • Mitophagy suppressed TGEV-induced oxidative stress and apoptosis.
  • TGEV upregulated DJ-1 and antioxidant genes.
  • Silencing DJ-1 inhibited mitophagy and increased apoptosis.
  • TGEV nucleocapsid protein (N) was found in mitochondria and mitophagosomes.

Conclusions:

  • TGEV infection activates mitophagy as a protective mechanism against oxidative stress and apoptosis.
  • DJ-1 plays a role in mediating TGEV-induced mitophagy.
  • The viral N protein localizes to mitochondria, suggesting a direct interaction.
  • Mitophagy may promote cell survival and facilitate TGEV infection.

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