| First Author | Matsuoka TA | Year | 2017 |
| Journal | Diabetes | Volume | 66 |
| Issue | 5 | Pages | 1293-1300 |
| PubMed ID | 28223284 | Mgi Jnum | J:247091 |
| Mgi Id | MGI:5922426 | Doi | 10.2337/db16-0887 |
| Citation | Matsuoka TA, et al. (2017) Mafa Enables Pdx1 to Effectively Convert Pancreatic Islet Progenitors and Committed Islet alpha-Cells Into beta-Cells In Vivo. Diabetes 66(5):1293-1300 |
| abstractText | Among the therapeutic avenues being explored for replacement of the functional islet beta-cell mass lost in type 1 diabetes (T1D), reprogramming of adult cell types into new beta-cells has been actively pursued. Notably, mouse islet alpha-cells will transdifferentiate into beta-cells under conditions of near beta-cell loss, a condition similar to T1D. Moreover, human islet alpha-cells also appear to poised for reprogramming into insulin-positive cells. Here we have generated transgenic mice conditionally expressing the islet beta-cell-enriched Mafa and/or Pdx1 transcription factors to examine their potential to transdifferentiate embryonic pan-islet cell Ngn3-positive progenitors and the later glucagon-positive alpha-cell population into beta-cells. Mafa was found to both potentiate the ability of Pdx1 to induce beta-cell formation from Ngn3-positive endocrine precursors and enable Pdx1 to produce beta-cells from alpha-cells. These results provide valuable insight into the fundamental mechanisms influencing islet cell plasticity in vivo. |
