Human liver regeneration following partial hepatectomy occurs primarily through normally
quiescent hepatocytes that undergo one or two rounds of replication, with restoration
of 70% of liver mass after 3-4 months. Liver injury induces a synchronized sequence
of events that proceed in an orderly manner with hepatocyte proliferation advancing
from the periportal to pericentral areas of the lobule. In contrast, liver repopulation
after acute liver failure depends on the differentiation of progenitor cells. Such
cells are also present in chronic liver diseases, but their contribution to the production
of hepatocytes in those conditions is unknown. We have previously demonstrated small
groups of histone positive cells that express stem cell markers Oct3/4, Nanog, Stat3,
and CD133 as well as TGF-β members, TGF-β receptor type 2 (TBR2) and ELF, at the end
of human liver regeneration at 4 months. Surprisingly, these cells dramatically lose
their phenotype to express Oct3/4, Nanog, Stat3, and CD133 but not TGF-β components
TBR2 or ELF in hepatocellular cancer (HCC) that often arises in the setting of chronic
liver injury. Moreover, genetic disruption of TGF-β signaling in elf+/− mice results in spontaneous HCC that can be reduced by reducing Stat3 signaling (PNAS
2008; 105:2445-2450).
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© 2009 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
