β-Cell Regeneration
Epithelial Mesenchymal Transition Pre-EMTpted by Lineage Tracing?
- 1Sarah W. Stedman Nutrition & Metabolism Center and Department of Medicine, Division of Endocrinology, Duke University Medical Center, Durham, North Carolina
- 2Section on Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Chicago, Chicago, Illinois
- Address correspondence to Prof. Christopher Rhodes, Research Director, Diabetes Center, University of Chicago, Department of Medicine–Endocrine Division, 5841 S. Maryland Ave, MC 1027, Room N138, Chicago, IL 60637. E-mail: cjrhodes{at}uchicago.edu
It is now appreciated that both type 1 and type 2 diabetes are diseases of β-cell insufficiency. As such, there is a good deal of interest in mechanisms of β-cell regeneration that hold some therapeutic potential (1). This could apply to increasing numbers of remaining endogenous β-cells in vivo, or in vitro expansion of β-cells derived from isolated human islets, to be subsequently used for β-cell replacement therapy. Regeneration of β-cells may occur by several means, including replication of existing β-cells, generation of new β-cells from pancreatic ductal precursor cells (by a relatively undefined mechanism known as neogenesis), and perhaps transdifferentiation of pancreatic exocrine cells into endocrine β-cells. It has also been suggested that some pancreatic cell types, including β-cells, can undergo a reversible epithelial-mesenchymal transition (EMT) to enable a marked increase in cell numbers (2,3). However, in this issue of Diabetes, Chase et al. (4), by use of lineage-tracing, demonstrate that EMT is unlikely to be a major source of β-cell regeneration.
What is EMT? Epithelial cells have a consistent and polarized morphology that are found in co-adherent organized multicellular assemblies, often in single-cell layers. In contrast, mesenchymal cells are of irregular shape, often with a spindle-like form characteristic of …
