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Functional characterization of ATP7B mutant hepatic cell lines after copper exposure
International Conference on Pediatric Gastroenterology and Pediatric Practices
Hartmut Schmidt
Universitatsklinikum Munster, Germany
Posters & Accepted Abstracts: J Gastrointest Dig Syst
Abstract
Wilson disease (WD) is caused by mutations of the ATP7B gene encoding a liver copper (Cu) transporter. The effect of anti-copper treatment for survival of hepatic cells expressing different ATP7B mutations is yet to be determined. The most common WD mutations p.H1069Q, p.R778L and p.C271* and mutations from Western India were studied. Expression of ATP7B, survival of cells, apoptosis and protein trafficking were determined. Low temperature increased ATP7B protein expression in several mutants. Intracellular ATP7B localization was significantly impaired in the mutants. Mutants were classified as high, moderate and no survival based on their viability on exposure to toxic copper. Survival of mutant p.H1069Q and to a lesser extent p.C271* improved by DPA treatment, while mutant p.R778L showed a pronounced response to Zn treatment. Overall, D-penicillamine (DPA) treatment resulted in higher cell survival as compared to Zn treatment; however, only combined Zn+DPA treatment fully restored cell viability. The data indicate that the basic impact of a genotype might be characterized by analysis of mutant hepatic cell lines.Biography
Email: hepar@ukmuenster.de
