Mapping a new therapeutic route can be fraught with challenges, but recent developments in the preparation and properties of small particles combined with significant improvements to tried and tested techniques offer refined cell targeting with tremendous translational potential. Regenerating new cells through the use of compounds that regulate epigenetic pathways represents an attractive approach that is gaining increased attention for the treatment of several diseases including Type 1 Diabetes and cardiomyopathy. However, cells that have been regenerated using epigenetic agents will still encounter immunological barriers as well as limitations associated with their longevity and potency during transplantation. Strategies aimed at protecting these epigenetically regenerated cells from the host immune response include microencapsulation. Microencapsulation can provide new solutions for the treatment of many diseases. In particular, it offers an advantageous method of administering therapeutic materials and molecules that cannot be substituted by pharmacological substances. Promising clinical findings have shown the potential beneficial use of microencapsulation for islet transplantation as well as for cardiac, hepatic, and neuronal repair. For the treatment of diseases such as type I diabetes that requires insulin release regulated by the patient's metabolic needs, microencapsulation may be the most effective therapeutic strategy. However, new materials need to be developed, so that transplanted encapsulated cells are able to survive for longer periods in the host. In this article, we discuss microencapsulation strategies and chart recent progress in nanomedicine that offers new potential for this area in the future.

Background Therapeutic replacement of pancreatic endocrine β-cells is key to improving hyperglycaemia caused by insulin-dependent diabetes . Whilst the pool of ductal progenitors, which give rise to the endocrine cells, are active during development, neogenesis of islets is repressed in the human adult. Recent human donor studies have demonstrated the role of EZH2 inhibition in surgically isolated exocrine cells showing reactivation of insulin expression and the influence on the H3K27me3 barrier to β-cell regeneration. However, those studies fall short on defining the cell type active in transcriptional reactivation events. This study examines the role of the regenerative capacity of human pancreatic ductal cells when stimulated with pharmacological inhibitors of the EZH2 methyltransferase. Results Human pancreatic ductal epithelial cells were stimulated with the EZH2 inhibitors GSK-126, EPZ6438, and triptolide using a 2- and 7-day protocol to determine their influence on the expression of core endocrine development marker NGN3, as well as β-cell markers insulin, MAFA, and PDX1. Chromatin immunoprecipitation studies show a close correspondence of pharmacological EZH2 inhibition with reduced H3K27me3 content of the core genes, NGN3, MAFA and PDX1. Consistent with the reduction of H3K27me3 by pharmacological inhibition of EZH2, we observe measurable immunofluorescence staining of insulin protein and glucose-sensitive insulin response. Conclusion The results of this study serve as a proof of concept for a probable source of β-cell induction from pancreatic ductal cells that are capable of influencing insulin expression. Whilst pharmacological inhibition of EZH2 can stimulate secretion of detectable insulin from ductal progenitor cells, further studies are required to address mechanism and the identity of ductal progenitor cell targets to improve likely methods designed to reduce the burden of insulin-dependent diabetes.