A controversial point in pancreas development is whether specialized mature cells in the adult organ are able to return to an earlier multipotent progenitor cell (MPC) state, and yield progeny that could replace cells damaged in disease states such as diabetes. In studies published Feb. 15 in Development, Fong Cheng Pan, Ph.D., Christopher Wright, D.Phil., and colleagues show the possibility of such “transdifferentiation” using a pancreatic injury model in mice.
The transcription factor Ptf1a is expressed in MPCs of the pancreas during early organ development, but later it is tightly restricted to acinar (digestive enzyme-secreting) cells. Using a genetic model to follow the progeny of adult acinar cells after injury, the researchers showed that some Ptf1a-positive acinar cells reverted to a multipotent state and produced apparently mature beta-cells – the insulin-secreting cells that are damaged in patients with diabetes.
The intrinsic multipotency and abundance of acinar cells in the pancreas make them a promising therapeutic target for controlled reprogramming within the patient’s own organ.
This research was supported by grants from the Juvenile Diabetes Research Foundation and the National Institutes of Health (DK042502, DK089570).
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