In the present review the authors discussed the identification of selector, or …

• Abstract
• Introduction
• Identification of master switch genes and MyoD
• Transdifferentiation of myoblasts to adipocytes
• In vivo pancreas to liver transdifferentiation
• Conversion of hepatic cells to pancreatic-like cells
• Transdifferentiation of liver to pancreas by ectopic expression of Pdx1
• Hes1 as a suppressor of Ngn3
• Wnt signalling
• Barrett's metaplasia
• Bone marrow transdifferentiation - fact or artefact?
• Summary
• References
• Figures

Biology Articles » Developmental Biology » The molecular basis of transdifferentiation » In vivo pancreas to liver transdifferentiation

In vivo pancreas to liver transdifferentiation

- The molecular basis of transdifferentiation

In vivo pancreas to liver transdifferentiation

Ectopic hepatic cells can be generated in the pancreas under a variety of conditions [19, 20]. Rao et al. treated rats with a copper depletion-repletion protocol and observed the appearance of multiple foci of hepatocytes in the pancreas [21]. The evidence for the presence of hepatocytes in the pancreas was based on the expression of albumin and catalase proteins although the molecular mechanisms mediating the switch in cell phenotype in this model remain elusive. Albumin and α- fetoprotein-positive cells have also been induced in the islets of Langerhans in transgenic mice expressing keratinocyte growth factor (KGF) under the control of the insulin promoter [22].

In vitro transdifferentiation of pancreatic cells to hepatocytes

More recently an in vitro model exhibiting the formation of transdifferentiated hepatocytes in pancreatic-derived AR42J-B13 cells (or B13 cells) has been described (Fig. 1A) and may provide some clues to the mechanisms underlying the changes observed in vivo [23–26]. The authors demonstrated that the transcription factor C/EBPβ is important for the transdifferentiation of pancreatic B13 cells to hepatocytes [23]. Over-expression of C/EBPβ induced the loss of the pancreatic phenotype and gain of the hepatic phenotype. The essential requirement for C/EBPβ in the transdifferentiation was shown by a dominant negative approach. Introduction of liver inhibitory protein (LIP), an alternative posttranscriptional product of C/EBPβ mRNA [27], prior to the treatment of B13 cells with dexamethasone, inhibited the induction of transdifferentiation.