Delayed apoptosis allows islet β-cells to implement an autophagic mechanism to promote cell survival.

ABSTRACT: Increased β-cell death coupled with the inability to replicate existing β-cells drives the decline in β-cell mass observed in the progression of both major forms of diabetes. Understanding endogenous mechanisms of islet cell survival could have considerable value for the development of novel strategies to limit β-cell loss and thereby promote β-cell recovery. Insulinoma cells have provided useful insight into β-cell death pathways but observations made in cell lines sometimes fail to translate to primary islets. Here, we report dramatic differences in the temporal regulation and engagement of the apoptotic program in primary rodent islets relative to the INS-1 derived 832/13 cell line. As expected, 832/13 cells rapidly induced cell stress markers in response to ER stress or DNA damage and

SUBMITTER: Hayes HL 

PROVIDER: S-EPMC5315295 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature