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Acute hypoxia induces apoptosis of pancreatic ß-cell by activation of the unfolded protein response and upregulation of CHOP.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zheng, X. Wang, X. Ma, Z. Gupta Sunkari, V. Botusan, I. Takeda, T. Björklund, A. Inoue, M. Catrina, S-B Brismar, K. Poellinger, L. Pereira, T. S.
Description	Country affiliation: Sweden Author Affiliation: Zheng X ( Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.)
Abstract	The success of pancreatic ß-cells transplantation to treat type 1 diabetes has been hindered by massive ß-cell dysfunction and loss of ß-cells that follows the procedure. Hypoxia-mediated cell death has been considered one of the main difficulties that must be overcome for transplantation to be regarded as a reliable therapy. Here we have investigated the mechanisms underlying ß-cell death in response to hypoxia (1% O(2)). Our studies show that mouse insulinoma cell line 6 (Min6) cells undergo apoptosis with caspase-3 activation occurring as early as 2 h following exposure to hypoxia. Hypoxia induces endoplasmic reticulum stress in Min6 cells leading to activation of the three branches of the unfolded protein response pathway. In response to hypoxia the pro-apoptotic transcription factor C/EBP homologous protein (CHOP) is upregulated. The important role of CHOP in the apoptotic process was highlighted by the rescue of Min6 cells from hypoxia-mediated apoptosis observed in CHOP-knockdown cells. Culturing isolated pancreatic mouse islets at normoxia showed intracellular hypoxia with accumulation of hypoxia-inducible factor-1 and upregulation of CHOP, the latter one occurring as early as 4 h after isolation. Finally, we observed that pancreatic islets of type 2 db/db diabetic mice were more hypoxic than their counterpart in normoglycemic animals. This finding indicates that hypoxia-mediated apoptosis may occur in type 2 diabetes.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2012.66
Journal	Cell Death and Disease
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2012-06-14
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Research Support, Non-u.s. Gov't Insulinoma Mice, Inbred C57bl Transcriptional Activation Mice, Transgenic Insulin-secreting Cells Metabolism Unfolded Protein Response Cell Hypoxia Discipline Cell Biology Animals Transcription Factor Chop Up-regulation Cell Line, Tumor Genetics Mice Apoptosis
Content Type	Text
Resource Type	Article

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