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Increased expression of ERp57/GRP58 is protective against pancreatic beta cell death caused by autophagic failure. | LitMetric

Increased expression of ERp57/GRP58 is protective against pancreatic beta cell death caused by autophagic failure.

Biochem Biophys Res Commun

Department of Metabolism and Endocrinology, Juntendo University, Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan; Center for Therapeutic Innovations in Diabetes, Juntendo University, Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan; Center for Molecular Diabetology, Juntendo University, Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. Electronic address:

Published: October 2014

AI Article Synopsis

  • - Autophagy is a process that helps pancreatic beta cells maintain balance and function, and its failure can negatively impact these cells.
  • - Research compared protein expressions in beta cells lacking Atg7 protein to normal cells, discovering that ERp57/GRP58 levels were higher in the deficient cells.
  • - Reducing ERp57 in beta cells led to increased cell death markers and changes in cell cycle patterns, suggesting that ERp57 might help protect against cell death when autophagy fails.

Article Abstract

Autophagy is a tightly regulated self-digestion system. As in other cell types, autophagy plays an essential role in the homeostasis of pancreatic beta cells. However, the mechanisms involved in the deterioration of beta cell function caused by autophagic failure have not yet been fully elucidated. To gain insight into its mechanisms, we compared the protein expression of islets from beta cell-specific Atg7-deficient mice (Atg7(Δβ-cell) mice) and their controls (Atg7(f/f) mice). Liquid chromatography/mass spectrometry after 1-dimensional electrophoresis identified the increased expression of ERp57/GRP58 in islets isolated from Atg7(Δβ-cell) mice compared with those from Atg7(f/f) mice. The expression level of ERp57 was also elevated in rat insulinoma INS-1 cells by inducible knock-down of the atg7-gene. In Atg7 knock-down INS-1 cells, the suppression of ERp57 expression by siRNA resulted in an increase in the level of cleaved Caspase-3 protein and a decrease in the number of live cells. Furthermore, cell cycle analyses demonstrated that the suppressed expression of ERp57 increased the sub-G1 population. These data reveal that increased expression of ERp57 may contribute to the protection from beta cell death caused by autophagic failure.

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Source
http://dx.doi.org/10.1016/j.bbrc.2014.09.040DOI Listing

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