No hepatic iron overload 12 years after liver transplantation for hereditary hemochromatosis
✍ Scribed by Marie-Pierre Bralet; Jean-Charles Duclos-Vallee; Denis Castaing; Didier Samuel; Catherine Guettier
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 88 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
An interesting report by Streetz et al. published in HEPATOLOGY described the production of hepatocyte conditional gp130 knockout mice subjected to chronic liver injury by repeated carbon tetrachloride (CCl 4 ) treatment. 1 Chronic injury induces liver regeneration by recruitment of cells from a precursor, either from a stem cell or a progenitor cell known as the oval cell. Numerous mouse studies such as that described by Streetz et al. 1 utilize albumin-alpha-fetoprotein (AFP) promoter and/or enhancer sequences to achieve hepatocyte specific gene deletions by expressing Cre recombinase. 2 The albumin-AFP promoter and/or enhancers are used, as AFP is an early marker of hepatocyte commitment. First detected at 8.5 days gestation in hepatoblasts, it is highly expressed in perinatal liver and diminishes to low or undetectable levels in the adult mouse. 3 Albumin production commences around 9.5 days gestation and is maintained throughout development. 4 We have previously shown that the choline-deficient, ethioninesupplemented diet (CDE) induces liver progenitor oval cells in rodents and that these cells express albumin and AFP. 5,6 Oval cells induced by CCl 4 will express albumin and AFP. 7 We therefore raise the possibility