NDLI: BILE SALT-INDUCED PRO-OXIDANT LIVER DAMAGE PROMOTES TRANSPLANTED CELL PROLIFERATION FOR CORRECTING WILSON DISEASE IN THE LEC RAT MODEL

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BILE SALT-INDUCED PRO-OXIDANT LIVER DAMAGE PROMOTES TRANSPLANTED CELL PROLIFERATION FOR CORRECTING WILSON DISEASE IN THE LEC RAT MODEL

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Joseph, Brigid Kapoor, Sorabh Schilsky, Michael L. Gupta, Sanjeev
Description	Country affiliation: United States Author Affiliation: Joseph B ( Marion Bessin Liver Research Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.)
Abstract	Insights into disease-specific mechanisms for liver repopulation are needed for cell therapy. To understand the efficacy of pro-oxidant hepatic perturbations in Wilson disease, we studied Long-Evans Cinnamon (LEC) rats with copper toxicosis under several conditions. Hepatocytes from healthy Long-Evans Agouti (LEA) rats were transplanted intrasplenically into the liver. A cure was defined as lowering of copper to below 250 microg/g liver, presence of ATPase, Cu++ transporting, beta polypeptide (atp7b) messenger RNA (mRNA) in the liver and improvement in liver histology. Treatment of animals with the hydrophobic bile salt, cholic acid, or liver radiation before cell transplantation produced cure rates of 14% and 33%, respectively; whereas liver radiation plus partial hepatectomy followed by cell transplantation proved more effective, with cure in 55%, P < 0.01; and liver radiation plus cholic acid followed by cell transplantation was most effective, with cure in 75%, P < 0.001. As a group, cell therapy cures in rats preconditioned with liver radiation plus cholic acid resulted in less hepatic copper, indicating greater extent of liver repopulation. We observed increased hepatic catalase and superoxide dismutase activities in LEC rats, suggesting chronic oxidative stress. After liver radiation or cholic acid, hepatic lipid peroxidation levels increased, indicating further oxidative injury, although we did not observe overt additional cytotoxicity. This contrasted with healthy animals in which liver radiation and cholic acid produced hepatic steatosis and loss of injured hepatocytes. We concluded that pro-oxidant perturbations were uniquely effective for cell therapy in Wilson disease because of the nature of preexisting hepatic damage.
File Format	HTM / HTML
ISSN	02709139
e-ISSN	15273350
DOI	10.1002/hep.22792
Journal	Hepatology
Issue Number	5
Volume Number	49
Language	English
Publisher	Wiley
Publisher Date	2009-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Hepatology Cell Proliferation Drug Effects Cholic Acid Pharmacology Hepatocytes Transplantation Hepatolenticular Degeneration Therapy Oxidative Stress Transplantation Conditioning Animals Copper Metabolism Rats, Inbred F344 Rats, Inbred Lec Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Hepatology

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BILE SALT-INDUCED PRO-OXIDANT LIVER DAMAGE PROMOTES TRANSPLANTED CELL PROLIFERATION FOR CORRECTING WILSON DISEASE IN THE LEC RAT MODEL

Repopulation of the fibrotic/cirrhotic rat liver by transplanted hepatic stem/progenitor cells and mature hepatocytes.

Hepatic irradiation augments engraftment of donor cells following hepatocyte transplantation.

Engraftment of syngeneic and allogeneic endothelial cells, hepatocytes and cholangiocytes into partially hepatectomized rats previously treated with mitomycin C.

Etanercept blocks inflammatory responses orchestrated by TNF- to promote transplanted cell engraftment and proliferation in rat liver.

Integration of transplanted hepatocytes into host liver plates demonstrated with dipeptidyl peptidase IV-deficient rats.

Gandou Decoction Decreases Copper Levels and Alleviates Hepatic Injury in Copper-Laden Hepatolenticular Degeneration Model Rats

Wilson disease.

Excess Copper and Ceruloplasmin Biosynthesis in Long-term Cultured Hepatocytes from Long-Evans Cinnamon (LEC) Rats, a Model of Wilson Disease

BILE SALT-INDUCED PRO-OXIDANT LIVER DAMAGE PROMOTES TRANSPLANTED CELL PROLIFERATION FOR CORRECTING WILSON DISEASE IN THE LEC RAT MODEL

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BILE SALT-INDUCED PRO-OXIDANT LIVER DAMAGE PROMOTES TRANSPLANTED CELL PROLIFERATION FOR CORRECTING WILSON DISEASE IN THE LEC RAT MODEL

Repopulation of the fibrotic/cirrhotic rat liver by transplanted hepatic stem/progenitor cells and mature hepatocytes.

Hepatic irradiation augments engraftment of donor cells following hepatocyte transplantation.

Engraftment of syngeneic and allogeneic endothelial cells, hepatocytes and cholangiocytes into partially hepatectomized rats previously treated with mitomycin C.

Etanercept blocks inflammatory responses orchestrated by TNF- to promote transplanted cell engraftment and proliferation in rat liver.

Integration of transplanted hepatocytes into host liver plates demonstrated with dipeptidyl peptidase IV-deficient rats.

Gandou Decoction Decreases Copper Levels and Alleviates Hepatic Injury in Copper-Laden Hepatolenticular Degeneration Model Rats

Wilson disease.

Excess Copper and Ceruloplasmin Biosynthesis in Long-term Cultured Hepatocytes from Long-Evans Cinnamon (LEC) Rats, a Model of Wilson Disease

BILE SALT-INDUCED PRO-OXIDANT LIVER DAMAGE PROMOTES TRANSPLANTED CELL PROLIFERATION FOR CORRECTING WILSON DISEASE IN THE LEC RAT MODEL