Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5861218 | Toxicology in Vitro | 2016 | 8 Pages |
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
ERADER-associated protein degradationshRNAsradioimmunoprecipitationThapsigarginLC3ATGRIPAPVDFFBSDMEMLPSDMSODulbecco's modified Eagle's mediumMTTDimethyl sulfoxidefetal bovine serumendoplasmic reticulumlipopolysaccharideHerpmicrotubule-associated protein 1 light chain 3Autophagy-related proteinsULDGlucose starvation
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Authors
Fenglei Chen, Pengfei Lin, Nan Wang, Diqi Yang, Xin Wen, Dong Zhou, Aihua Wang, Yaping Jin,