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mortl/fadd is involved in liver regeneration

World Journal of Gastroenterology 2005年第46期11卷 7248-7253页

作者： Marcus Schuchmann Felix Rückert Jose F Garcia-Lazaro Andrea Karg Jürgen Burg Natalia Knorr Jürgen Siebler Eugene E Varfolomeev David Wallach Wolfgang Schreiber Ansgar W Lohse Peter R Galle Department of Medicine University of Mainz Langenbeckstr.1Mainz 55101 Germany Institute of RadiologyUniversity of Mainz Langenbeckstr.1Mainz 55101Germany Institute of PathologyUniversity of Mainz Langenbeckstr. 1 Mainz 55101 Germany Department of MedicineUniversity of Mainz Langenbeckstr.1Mainz 55101Germany GenentechSouth San Francisco CAUnited States The Weizmann Institute of ScienceRehovot Israel Institute of RadiologyUniversity of Mainz Langenbeckstr.1Mainz 55101 Germany Department of Medicine University of Mainz Langenbeckstr.1Mainz 55101 Germany

AIM: To explore the role of the adaptor molecule in liver regeneration after partial hepatectomy (PH). METHODS: We used transgenic mice expressing an N-terminal truncated form of mort1/fadd under the control of the albumin promoter. As previously shown, this transgenic protein abrogated CD95- and CD120a-mediated apoptosis in the liver. Cyclin A expression was detected using Western blotting. ELISA and RT-PCR were used to detect IL-6 and IL-6 mRNA, respectively. DNA synthesis in liver tissue was measured by BrdU staining. RESULTS: Resection of 70% of the liver was followed by a reduced early regenerative response in the transgenic group at 36 h. Accordingly, 36 h after hepatectomy, cyclin A expression was only detectable in wild-type animals. Consequently, the onset of liver mass restoration was retarded as measured by MRI volumetry and mortality was significantly higher in the transgenic group. CONCLUSION: Our data demonstrate for the first time an involvement of the death receptor molecule mort1/ fadd in liver regeneration, beyond its well described role as part of the intracellular death signaling pathway.

关键词： mort1/fadd CD95 TNF Apoptosis Liver regeneration

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