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成纤维细胞生长因子-2缺乏小鼠的肝脏再生：血管内皮生长因子可作为成纤维细胞生长因子-2的潜在功能替代物。

Liver regeneration in FGF-2-deficient mice: VEGF acts as potential functional substitute for FGF-2.

作者信息

Sturm Jörg, Keese Michael, Zhang Honyue, Bönninghoff Roderich, Magdeburg Richard, Vajkoczy Peter, Dono Rosanna, Zeller Rolf, Gretz Norbert

机构信息

Chirurgische Klinik, Universitätsklinikum Mannheim, Germany.

出版信息

Liver Int. 2004 Apr;24(2):161-8. doi: 10.1111/j.1478-3231.2004.0896.x.

DOI:10.1111/j.1478-3231.2004.0896.x
PMID:15078481
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.

摘要

背景/目的：血管生成特性、其在中胚层分化中的作用以及细胞培养研究表明，成纤维细胞生长因子（FGF-2）在肝脏再生中起重要作用。本研究旨在评估FGF-2基因敲除小鼠模型中的这一作用。

方法

对纯合FGF-2缺陷型（-/-）小鼠（雄性C57BL/6J）及其FGF-2功能正常的（+/+）同窝小鼠（对照）进行左半肝切除术后（部分肝切除术，PH）的肝脏再生评估（第0 - 10天）。

结果

FGF-2（-/-）小鼠在肝脏再生中表现出正常动态。对照小鼠在PH后4天FGF-2蛋白过度表达。BrdU掺入在FGF-2（-/-）小鼠中呈双相模式，而在对照小鼠中，在一个峰值（第2天）后持续下降。与对照相比，FGF-2（-/-）肝脏中PH后肝生长因子mRNA下降时间延长1天，此后升高明显较少。与对照相反，FGF-2（-/-）小鼠术前和术后血管内皮生长因子（VEGF）mRNA水平明显升高。FGF-2（-/-）小鼠肝脏中的VEGF蛋白水平术前升高，但PH后两组相似。使用VEGF受体抑制剂SU5416，FGF-2（-/-）小鼠的肝脏再生显著降低，而对照小鼠则保持不变。

结论

FGF-2（-/-）小鼠的肝脏再生动态与对照相当，这可能是由于VEGF对FGF-2的功能替代。

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