The transcription factor STAT6 plays a critical role in promoting beta cell viability and is depleted in islets of individuals with type 1 diabetes.

摘要: In type 1 diabetes, selective beta cell loss occurs within the inflamed milieu of insulitic islets. This is generated via enhanced secretion proinflammatory cytokines and by anti-inflammatory molecules such as IL-4 IL-13. While actions have been well-studied in cells, effects their counterparts received relatively little attention we addressed this. Clonal isolated human islets pancreas sections from control individuals those with diabetes were employed. Gene expression was measured using targeted gene arrays quantitative RT-PCR. Protein monitored extracts western blotting tissue immunocytochemistry. Target proteins knocked down selectively interference RNA. Cytoprotection achieved IL-13 mediated early activation signal transducer activator transcription 6 (STAT6) leading to upregulation anti-apoptotic proteins, including myeloid leukaemia-1 (MCL-1) B lymphoma-extra large (BCLXL). We also report induction regulatory protein-α (SIRPα), find that knockdown SIRPα associated reduced viability. These attendant cytoprotective are lost following siRNA-mediated STAT6 cells. Importantly, analysis revealed markedly depleted cells implying responses. Selective may contribute demise during progression diabetes.