Federal Regulation of Embryonic Stem Cells: Can Government Do It - An Examination of Potential Regulation through the Eyes of California\u27s Recent Legislation

The debate surrounding stem cell research, particularly embryonic stem cell research, is one involving much acrimony, both at the research and practical stages. Such research holds the potential for abuse if not responsibly undertaken. This does not mean, however, that embryonic stem cell research should be prohibited subject to the whims of opponents in Congress. Rather, California has taken the proper step by endorsing embryonic stem cell research, while maintaining guidelines to oversee it

All-trans retinoic acid suppresses exocrine differentiation and branching morphogenesis in the embryonic pancreas

Recent evidence has shown that retinoic acid (RA) signalling is required for early pancreatic development in zebrafish and frog but its role in later development in mammals is less clear cut. In the present study, we determined the effects of RA on the differentiation of the mouse embryonic pancreas. Addition of all-trans retinoic acid (atRA) to embryonic pancreatic cultures induced a number of changes. Branching morphogenesis and exocrine differentiation were suppressed and there was premature formation of endocrine cell clusters (although the total area of β cells was not different in control and atRA-treated buds). We investigated the mechanism of these changes and found that the premature formation of β cells was associated with the early expression of high-level Pdx1 in the endocrine cell clusters. In contrast, the suppressive effect of RA on exocrine differentiation may be due to a combination of two mechanisms (i) up-regulation of the extracellular matrix component laminin and (ii) enhancement of apoptosis. We also demonstrate that addition of fibroblast growth factor (FGF)-10 is able to partially prevent apoptosis and rescue exocrine differentiation and branching morphogenesis in atRA-treated cultures but not in mice lacking the FGF receptor 2-IIIb, suggesting the effects of FGF-10 are mediated through this receptor