Researchers have discovered the barrier to β-cell regeneration that could pave the way for improved treatments for diabetes and diseases that involve organ and tissue damage. This process is regulated by methylation changes of two key developmental genes Ngn3 and Sox 11. They have been known before, the recent study demonstrated how exactly regulation of these two genes affects diabetes symptoms.
Currently, replacing the damaged β-cell mass in diabetic patients consists of whole pancreas or islets transplantation. Although efficient, these therapies face the shortage of organ donors together with the associated side effects of immunosuppressive drugs. The recent study focuses on the replacement of the lost β-cells in diabetic patients using several approaches and cell sources. However, critical to exploiting the potential of these regenerative approaches, is understanding how tissue and cellular processes are controlled during development.Discovered mechanisms may become a basis for potential new diabetes treatment, including diabetes type 1 and type 2.
DNA methylation status correlates with adult β-cell regeneration capacity
The role of DNA methylation in β-cell neogenesis is poorly understood. We report that during the process of induced cell reprogramming, methylation content of the Ngn3 and Sox11 genes are diminished. These findings emphasise DNA methylation is a barrier in β-cell regeneration in adulthood, a well described pathophysiological phenomenon of major significance in explaining β-cell deficiency in diabetes in the adult pancreas.