According to the study, published in the journal npj Regenerative Medicine, the human body doesn't repair itself very well, with our liver the only organ that can regenerate efficiently as we have limited capacity to regenerate new cells or tissue after birth as the genes involved in development are switched off.
This process happens through DNA methylation, a biological process where chemicals (methyl groups) are written on DNA and modify the way the gene functions, said the researchers, including Sam El-Osta from Monash University. This modification effectively silences genes of progenitor cells (early descendants of stem cells) in the body and thereby the ability for the pancreas to generate the insulin-producing beta cells, they added.
The research team, using mouse models, found that the DNA methylation content of two key developmental genes Ngn3 and Sox 11 were diminished, effectively making them 'repair' dormant. However, through demethylation, progenitor cells can be reawakened, restoring their capacity to become new insulin-producing beta cells paving the way towards improved treatments for Type-1 and Type-2 diabetes, the team said.
"The discovery that DNA methylation is a barrier to adult beta-cell regeneration will assist scientists to restore beta-cell function in the pancreas," said Professor El-Osta. Currently, replacing the damaged beta-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 team said.
Current research focuses on the replacement of the lost beta 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.