CCl4‐induced acute liver injury in mice is inhibited by hepatocyte growth factor overexpression but stimulated by NK2 overexpression

FEBS Letters

Mori, Masatomo¹  Takagi, Hitoshi¹  Toyoda, Mitsuo¹  Takayama, Hisashi¹  Otsuka, Toshiyuki¹  Horiguchi, Norio¹  Sato, Ken¹ 

[1] First Department of Internal Medicine, Gunma University School of Medicine, 3-39-15 Showa, Maebashi, Gunma 371-8511, Japan

关键词: Hepatocyte growth factor;    NK2;    Transgenic mouse;    Carbon tetrachloride;    Liver injury;    Hepatocyte proliferation;    HGF;    hepatocyte growth factor;    CCl4;    carbon tetrachloride;    MT;    metallothionein;    WT;    wild-type;    ZnSO4;    zinc sulfate;    ALT;    alanine aminotransferase;    GAPDH;    glyceraldehyde-3-phosphate dehydrogenase;    PCNA;    proliferating cell nuclear antigen;    ANOVA;    analysis of variance;   

DOI  :  10.1016/S0014-5793(02)03714-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Hepatocyte growth factor (HGF) inhibits acute liver injury. NK2 acts as an antagonist to HGF in vitro, but its in vivo function has reached no consensus conclusions. We have investigated in vivo effects of HGF and NK2 on CCl₄-induced acute liver injury. Elevation of the serum alanine aminotransferase level and extension of centrilobular necrosis were inhibited in HGF transgenic mice but were promoted in NK2 transgenic mice. Hepatocyte proliferation after liver injury was not inhibited in NK2 transgenic mice. Thus, this study indicates that HGF inhibits liver injury, and NK2 antagonizes HGF on liver injury, however, NK2 may not antagonize HGF on hepatocyte proliferation.

【 授权许可】

Unknown