Liver regeneration in FGF-2-deficient mice

• Verfasst von: Sturm, Jörg [VerfasserIn]
• Verfasst von: Keese, Michael [VerfasserIn]
• Verfasst von: Zhang, Honyue [VerfasserIn]
• Verfasst von: Bönninghoff, Roderich [VerfasserIn]
• Verfasst von: Magdeburg, Richard [VerfasserIn]
• Verfasst von: Vajkoczy, Peter [VerfasserIn]
• Verfasst von: Dono, Rosanna [VerfasserIn]
• Verfasst von: Zeller, Rolf [VerfasserIn]
• Verfasst von: Gretz, Norbert [VerfasserIn]
• Titel: Liver regeneration in FGF-2-deficient mice
• Titelzusatz: VEGF acts as potential functional substitute for FGF-2
• Verf.angabe: Jörg Sturm, Michael Keese, Honyue Zhang, Roderich Bönninghoff, Richard Magdeburg, Peter Vajkoczy, Rosanna Dono, Rolf Zeller, Norbert Gretz
• E-Jahr: 2004
• Jahr: 01 April 2004
• Umfang: 8 S.
• Illustrationen: Illustrationen
• Fussnoten: Gesehen am 22.06.2022
• Titel Quelle: Enthalten in: Liver international
• Ort Quelle: Oxford : Wiley-Blackwell, 2003
• Jahr Quelle: 2004
• Band/Heft Quelle: 24(2004), 2, Seite 161-168
• ISSN Quelle: 1478-3231
• DOI: doi:10.1111/j.1478-3231.2004.0896.x
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: angiogenesis
• Sach-SW: bFGF
• Sach-SW: FGF-2
• Sach-SW: FGF-2 deficient mice
• Sach-SW: HGF
• Sach-SW: liver regeneration
• Sach-SW: VEGF
• K10plus-PPN: 1807456609

Abstract

Background/Aims: The angiogenic properties, its role in mesoderm differentiation and cell culture studies implicate an important role of fibroblast growth factor (FGF-2) in liver regeneration. The aim of the study was to evaluate this role in a FGF-2 knockout mouse model. Methods: Liver regeneration after left hemihepatectomy (partial hepatectomy, PH) was evaluated in homozygous FGF-2 deficient (−/−) mice (male C57BL/6J) and their FGF-2 competent (+/+) littermates (controls) (day 0-10). Results: FGF-2-(−/−) mice displayed normal dynamics in liver regeneration. FGF-2 protein was overexpressed 4 days post PH in controls. BrdU incorporation showed a biphasic pattern in FGF-2-(−/−) mice, whereas it decreased continuously after one peak (day 2) in controls. In FGF-2-(−/−) livers hepatic growth factor mRNA post PH was 1 day longer decreased and markedly less elevated thereafter compared with control. Vascular endothelial growth factor (VEGF) mRNA levels were clearly increased in FGF-2-(−/−) mice pre- and postoperatively in contrast to controls. VEGF protein levels in livers of FGF-2-(−/−) mice were elevated preoperatively, but similar in both groups after PH. With SU5416, a VEGF-receptor inhibitor, liver regeneration in FGF-2-(−/−) mice was reduced significantly, whereas it remained unchanged in controls. Conclusions: Liver regeneration dynamics in FGF-2-(−/−) mice were comparable with controls, potentially due to a functional substitution of FGF-2 by VEGF.