Tokyo, Japan -
Embryonic stem cells have a very high potential to generate various tissues, a potential so high that it actually serves as a drawback in some senses. See, embryonic stem cells, when grown in floating cultures form embryoid bodies, and in these embryoid bodies the embryonic stem cell starts differentiating into a wide variety of different tissues spontaneously.
There are patents out there that teach people to "fish out" specific cells from the spontaneously differentiating embryonic stem cells through the use of surface markers or activation of a promotor. There are also patents on how to selectively push differentiation of the stem cell towards one lineage or another, for example into cardiac, brain, or pancreatic tissues. However it is still difficult to reproducibly generate specific tissues from the embryonic stem cells.
In a recent paper (Fujimori et al. Vascular endothelial growth factor promotes proliferation and function of hepatocyte-like cells in embryoid bodies formed from mouse embryonic stem cells. J Hepatol. 2008 Mar 10) scientists tried to figure out how to make more hepatocytes in embryoid bodies.
The scientists generated embryoid bodies and added the proangiogenic protein VEGF, additionally they added inhibitors of the VEGF receptor to demonstrate importance of the cytokine in expansion of liver like cells within the embryoid body. They found:
- Addition of VEGF to embryoid bodies increased the number of endothelial cells in the embryoid bodies, as well as the number of hepatic-like cells
- The VEGF inhibitor suppressed the number of hepatic-like cells, as well as their production of albumin and HGF
These data suggest that the presence of endothelial cells is associated with increased differentiation of embryonic stem cells into hepatocytes. One wonders if in the adult situation whether stimulation of angiogenesis would also augment liver cell regeneration? This is of particular interest since it has been published that clinical administration of autologous bone marrow is associated with increased hepatic regeneration in patients with liver failure. Maybe the hepatic regeneration has nothing to do with transdifferentiation but simply augmentation of angiogenesis in the hepatic environment.
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