Reprogramming Cells: Challenges Remain

Type 1 diabetes results from the loss of insulin-producing beta cells in the pancreas. One potential way to cure the disease is to “reprogram” pancreatic acinar cells, which normally produce proteolytic enzymes, so that they start producing insulin instead.

This is easier said than done. In a report published last month in the journal Cell Reports, graduate student Hannah Clayton, Mark Magnuson, M.D., and colleagues describe how the conversion of acinar into beta cells into depends on both the concentration of a triad of reprogramming transcription factors and the level of inflammation.

Overly robust expression of these factors induces induce pancreatic inflammation, which blocks apartment reprogramming and results instead in production of duct-like cells. Only when inflammation is attenuated, by reducing transcription of factor expression or by depending inflammatory macrophages, does production of new beta-like cells occur.

For in vivo beta-cell restorative therapy to become clinically feasible, it will necessary to understand more the fully the complex and coordinated series of events that modulate intercellular, the researchers concluded.

The Reporter: Vanderbilt University Medical Center’s Weekly Newspaper

Friday, December 9th, 2016

Bill Snyder

Record History
Added on June 19, 2014 at 1:53 PM by Ray, Terri
Modified on February 3, 2017 at 3:24 PM by Ray, Terri
Shared with (contributions)
Public: Shared Collection
DRTC: Vanderbilt Diabetes: Prior Featured Investigators Master

Pancreatic Inflammation Redirects Acinar to β Cell Reprogramming.
Clayton HW, Osipovich AB, Stancill JS, Schneider JD, Vianna PG, Shanks CM,
Yuan W, Gu G, Manduchi E, Stoeckert CJ, Magnuson MA (2016) Cell Rep 17(8): 2028-2041

Primary Publication:
27851966 (PubMed)

PMC5131369 (PubMed Central)


Mark A. Magnuson and Hannah W. Clayton »
Hannah, a graduate student, is the first author of the Featured Publication.