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1 Marion Bessin Liver Research Center, 2 Cancer Research Center, Departments of 3 Medicine, 4 Pediatrics, 5 Microbiology and Immunology, and 6 Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, New York 10461
To understand
regulation of transplanted hepatocyte proliferation in the normal
liver, we used genetically marked rat or mouse cells. Hosts were
subjected to liver injury by carbon tetrachloride (CCl4),
to liver regeneration by a two-thirds partial hepatectomy, and to
hepatocellular DNA synthesis by infusion of hepatocyte growth factor
for comparative analysis. Transplanted hepatocytes were documented to
integrate in periportal areas of the liver. In response to
CCl4 treatments after cell transplantation, the transplanted hepatocyte mass increased incrementally, with the kinetics
and magnitude of DNA synthesis being similar to those of host
hepatocytes. In contrast, when cells were transplanted 24 h after
CCl4 administration, transplanted hepatocytes appeared to
be injured and most cells were rapidly cleared. When hepatocyte growth
factor was infused into the portal circulation either subsequent to or
before cell transplantation and engraftment, transplanted cell mass did
not increase, although DNA synthesis rates increased in cultured
primary hepatocytes as well as in intact mouse and rat livers. These
data suggested that procedures causing selective ablation of host
hepatocytes will be most effective in inducing transplanted cell
proliferation in the normal liver. The number of transplanted
hepatocytes was not increased in the liver by hepatocyte growth factor
administration. Repopulation of the liver with genetically marked
hepatocytes can provide effective reporters for studying liver growth
control in the intact animal.
carbon tetrachloride; hepatocyte transplantation; liver regeneration
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