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http://purl.uniprot.org/citations/15078481http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15078481http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.org/dc/terms/identifier"doi:10.1111/j.1478-3231.2004.0896.x"xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Gretz N."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Keese M."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Sturm J."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Vajkoczy P."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Zeller R."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Dono R."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Bonninghoff R."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/author"Magdeburg R."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/name"Liver Int"xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/pages"161-168"xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/title"Liver regeneration in FGF-2-deficient mice: VEGF acts as potential functional substitute for FGF-2."xsd:string
http://purl.uniprot.org/citations/15078481http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/15078481http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15078481
http://purl.uniprot.org/citations/15078481http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15078481
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