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A different transformation

Transcription factor and liver-specific mRNA expression in facultative epithelial progenitor cells of liver and pancreas Dabeva MD, Hurston E and Shafritz DA American Journal of Pathology 1995; 147: 1633- 1648

School of Biological Sciences University of Surrey, Guildford GU2 SXH, UK

The pattern of mRNA expression for liver-specific proteins and liver-enriched transcription factors were studied in two models of facultative gut epithelial progenitor cells activation: D-galactosa mine (GalN)-induced liver injury and dietary copper depletion leading to pancreatic acinar atrophy. After 5 weeks of copper deficiency (CuD, pancreatic acini of Fischer 344 rats underwent atrophy, associated with intense proliferation of small ductlike cells with oval-shaped nuclei. These cells resemble morphologically epithelial progenitor cells of the liver that proliferate after GalN administration. Activated pancreatic epithelial cells express mRNAs for five liver specific genes normally expressed in fetal liver, including 1 antitrypsin, glucose-6-phosphatase, and others, but not genes that are turned on after birth such as serine dehydratase, tyrosine aminotransferase, and multidrug resistance gene-1b. They express mRNAs for liver-enriched transcription factors including HNF-1, HNF-3β and , HNF-4, and members of the CCAAT-enhancer binding protein (C/EBP) family. The only mRNA for a liver-enriched transcription factor not detected in the pancreas of CuD animals was HNF-3. Expression of HNF-3, β and , and C/EBP-β mRNA was highly activated in proliferating liver epithelial cells on days 2 and 3 after GalN injury. Increased expression of C/EBP- was observed first in the liver on day 1 after GalN administration and in the pancreas at 4 weeks after initiating CuD. We suggest that C/EBP- could not be involved in the initial activation of epithelial progenitor cells and that HNF-3, β and , and C/EBP-β might participate in their maturation. We conclude further that pancreatic epithelial progeni tor cells undertake differentiation through the hepatocyte lineage but cannot complete the differ entiation program within the pancreatic milieu.

Human & Experimental Toxicology, Vol. 15, No. 6, 541-543 (1996)
DOI: 10.1177/096032719601500615


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