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. 2008 Jan;28(1):126-31.
doi: 10.1111/j.1478-3231.2007.01616.x. Epub 2007 Nov 1.

Overexpression of NK2 promotes liver fibrosis in carbon tetrachloride-induced chronic liver injury

Satoshi Hagiwara  1 , Toshiyuki Otsuka, Yuichi Yamazaki, Takashi Kosone, Naondo Sohara, Takeshi Ichikawa, Ken Sato, Satoru Kakizaki, Hitoshi Takagi, Masatomo Mori
Affiliations

Overexpression of NK2 promotes liver fibrosis in carbon tetrachloride-induced chronic liver injury

Satoshi Hagiwara et al. Liver Int. 2008 Jan.

Erratum in

  • Liver Int. 2008 Apr;28(4):582

Abstract

Background/aims: Hepatocyte growth factor (HGF) inhibits liver fibrosis induced by carbon tetrachloride (CCl4) in animal models. NK2 is a natural splice variant of HGF, but its in vivo function remains to be elucidated. We investigated the in vivo effects of NK2 on CCl4-induced liver fibrosis.

Methods: NK2 transgenic mice and wild-type (WT) mice were injected intraperitoneally with CCl4 twice a week. The extent of hepatic fibrosis was evaluated by Azan-Mallory staining. Expression levels of mRNAs of transforming growth factor-beta1 (TGF-beta1) and matrix metalloproteinase-13 (MMP-13) were examined by real-time polymerase chain reaction. The protein levels of alpha-smooth muscle actin (alpha-SMA), c-Met and its phosphorylation were determined by Western blot analysis.

Results: Liver fibrosis was significantly more severe in NK2 transgenic mice than in WT mice. CCl4 administration increased the expression levels of TGF-beta1 mRNA and alpha-SMA protein, and decreased the expression of MMP-13 mRNA in livers of NK2 transgenic mice compared with those of WT mice. c-Met protein expression in the liver was compatible with the degree of fibrosis. As for c-Met activation, no difference was found between NK2 and WT livers.

Conclusion: Overexpression of NK2 acts as an antagonist of HGF and promotes liver fibrosis in CCl4-induced chronic liver injury.

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