| First Author | Clayton HW | Year | 2016 |
| Journal | Cell Rep | Volume | 17 |
| Issue | 8 | Pages | 2028-2041 |
| PubMed ID | 27851966 | Mgi Jnum | J:241149 |
| Mgi Id | MGI:5897923 | Doi | 10.1016/j.celrep.2016.10.068 |
| Citation | Clayton HW, et al. (2016) Pancreatic Inflammation Redirects Acinar to beta Cell Reprogramming. Cell Rep 17(8):2028-2041 |
| abstractText | Using a transgenic mouse model to express MafA, Pdx1, and Neurog3 (3TF) in a pancreatic acinar cell- and doxycycline-dependent manner, we discovered that the outcome of transcription factor-mediated acinar to beta-like cellular reprogramming is dependent on both the magnitude of 3TF expression and on reprogramming-induced inflammation. Overly robust 3TF expression causes acinar cell necrosis, resulting in marked inflammation and acinar-to-ductal metaplasia. Generation of new beta-like cells requires limiting reprogramming-induced inflammation, either by reducing 3TF expression or by eliminating macrophages. The new beta-like cells were able to reverse streptozotocin-induced diabetes 6 days after inducing 3TF expression but failed to sustain their function after removal of the reprogramming factors. |
