| First Author | Yamaoka T | Year | 2002 |
| Journal | Biochem Biophys Res Commun | Volume | 292 |
| Issue | 1 | Pages | 138-43 |
| PubMed ID | 11890684 | Mgi Jnum | J:75690 |
| Mgi Id | MGI:2177373 | Doi | 10.1006/bbrc.2002.6601 |
| Citation | Yamaoka T, et al. (2002) Transgenic expression of FGF8 and FGF10 induces transdifferentiation of pancreatic islet cells into hepatocytes and exocrine cells. Biochem Biophys Res Commun 292(1):138-43 |
| abstractText | FGF signaling is essential for normal development of pancreatic islets. To examine the effects of overexpressed FGF8 and FGF10 on pancreatic development, we generated FGF8- and FGF10-transgenic mice (Tg mice) under the control of the glucagon promoter. In FGF8-Tg mice, hepatocyte-like cells were observed in the periphery of pancreatic islets, but areas of alpha and beta cells did not decrease, whereas in FGF10-Tg mice, pancreatic ductal and acinar cells were found in islets, concomitantly with disturbed beta-cell differentiation. These results suggest that FGF8 and FGF10 play important roles in development of hepatocytes and exocrine cells, respectively, and explain the absence of FGF8 expression in normal islets and pancreatic hypoplasia in FGF10-deficient mice. |
