Herp depletion inhibits zearalenone-induced cell death in RAW 264.7 macrophages

Toxicol In Vitro. 2016 Apr:32:115-22. doi: 10.1016/j.tiv.2015.12.014. Epub 2015 Dec 23.

Abstract

Herp is an endoplasmic reticulum (ER) membrane protein and strongly induced by the ER stress that not only participates in the unfolded protein response (UPR) under the ER stress, but also in cell autophagy under glucose starvation (GS). However, we do not know whether Herp plays any roles in other responses, such as zearalenone (ZEA). In this study, we constructed recombinant lentiviral vectors for Herp shRNA expression and generated stable Herp knockdown RAW 264.7 macrophages. Flow cytometry analysis showed Herp depletion could inhibit cell death induced by ZEA. Western blot analysis revealed that Herp depletion could up-regulate autophagy-related protein LC3-I conversion into LC3-II and the expression of ER stress-related protein CHOP. These results suggest that Herp depletion inhibits cell death by up-regulating autophagy.

Keywords: Autophagy; Cell death; Herp; LC3; Zearalenone.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death / drug effects
  • Cell Line
  • Cell Survival / drug effects
  • Endoplasmic Reticulum Chaperone BiP
  • Heat-Shock Proteins / metabolism
  • Lentivirus / genetics
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Mice
  • Microtubule-Associated Proteins / metabolism
  • RNA, Small Interfering / genetics
  • Transcription Factor CHOP / metabolism
  • Zearalenone / toxicity*

Substances

  • Ddit3 protein, mouse
  • Endoplasmic Reticulum Chaperone BiP
  • Heat-Shock Proteins
  • Herpud1 protein, mouse
  • Map1lc3b protein, mouse
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • RNA, Small Interfering
  • Transcription Factor CHOP
  • Zearalenone