HDLs protect the MIN6 insulinoma cell line against tunicamycin-induced apoptosis without inhibiting ER stress and without restoring ER functionality.
Details
State: Public
Version: Author's accepted manuscript
Serval ID
serval:BIB_C9C6FBEF97BF
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
HDLs protect the MIN6 insulinoma cell line against tunicamycin-induced apoptosis without inhibiting ER stress and without restoring ER functionality.
Journal
Molecular and Cellular Endocrinology
ISSN
1872-8057 (Electronic)
ISSN-L
0303-7207
Publication state
Published
Issued date
2013
Peer-reviewed
Oui
Volume
381
Number
1-2
Pages
291-301
Language
english
Abstract
HDLs protect pancreatic beta cells against apoptosis induced by several endoplasmic reticulum (ER) stressors, including thapsigargin, cyclopiazonic acid, palmitate and insulin over-expression. This protection is mediated by the capacity of HDLs to maintain proper ER morphology and ER functions such as protein folding and trafficking. Here, we identified a distinct mode of protection exerted by HDLs in beta cells challenged with tunicamycin (TM), a protein glycosylation inhibitor inducing ER stress. HDLs were found to inhibit apoptosis induced by TM in the MIN6 insulinoma cell line and this correlated with the maintenance of a normal ER morphology. Surprisingly however, this protective response was neither associated with a significant ER stress reduction, nor with restoration of protein folding and trafficking in the ER. These data indicate that HDLs can use at least two mechanisms to protect beta cells against ER stressors. One that relies on the maintenance of ER function and one that operates independently of ER function modulation. The capacity of HDLs to activate several anti-apoptotic pathways in beta cells may explain their ability to efficiently protect these cells against a variety of insults.
Pubmed
Web of science
Open Access
Yes
Create date
03/10/2013 9:46
Last modification date
20/08/2019 16:44