| First Author | Yuchi Y | Year | 2015 |
| Journal | Diabetes | Volume | 64 |
| Issue | 9 | Pages | 3218-28 |
| PubMed ID | 26015547 | Mgi Jnum | J:246946 |
| Mgi Id | MGI:5923861 | Doi | 10.2337/db14-1798 |
| Citation | Yuchi Y, et al. (2015) Estrogen Receptor alpha Regulates beta-Cell Formation During Pancreas Development and Following Injury. Diabetes 64(9):3218-28 |
| abstractText | Identifying pathways for beta-cell generation is essential for cell therapy in diabetes. We investigated the potential of 17beta-estradiol (E2) and estrogen receptor (ER) signaling for stimulating beta-cell generation during embryonic development and in the severely injured adult pancreas. E2 concentration, ER activity, and number of ERalpha transcripts were enhanced in the pancreas injured by partial duct ligation (PDL) along with nuclear localization of ERalpha in beta-cells. PDL-induced proliferation of beta-cells depended on aromatase activity. The activation of Neurogenin3 (Ngn3) gene expression and beta-cell growth in PDL pancreas were impaired when ERalpha was turned off chemically or genetically (ERalpha(-/-)), whereas in situ delivery of E2 promoted beta-cell formation. In the embryonic pancreas, beta-cell replication, number of Ngn3(+) progenitor cells, and expression of key transcription factors of the endocrine lineage were decreased by ERalpha inactivation. The current study reveals that E2 and ERalpha signaling can drive beta-cell replication and formation in mouse pancreas. |
