TNFR1-mediated signaling is important to induce the improvement of liver fibrosis by bone marrow cell infusion

被引:9
作者
Hisanaga, Takuro [1 ]
Terai, Shuji [1 ]
Iwamoto, Takuya [1 ]
Takami, Taro [1 ]
Yamamoto, Naoki [1 ]
Murata, Tomoaki [2 ]
Matsuyama, Toshifumi [3 ]
Nishina, Hiroshi [4 ]
Sakaida, Isao [1 ]
机构
[1] Yamaguchi Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Yamaguchi 7558505, Japan
[2] Yamaguchi Univ, Inst Lab Anim, Yamaguchi 7558505, Japan
[3] Nagasaki Univ, Grad Sch Biomed Sci, Dept Mol Microbiol & Immunol, Nagasaki 8528523, Japan
[4] Tokyo Med & Dent Univ, Med Res Inst, Dept Dev & Regenerat Biol, Bunkyo Ku, Tokyo 1130034, Japan
基金
日本科学技术振兴机构; 日本学术振兴会;
关键词
Tumor necrosis factor; CCl(4); Bone marrow cell; Liver cirrhosis; Hepatic stellate cell; NECROSIS-FACTOR RECEPTOR; CARBON-TETRACHLORIDE; HEPATIC-FIBROSIS; FACTOR-ALPHA; TNF-ALPHA; MATRIX METALLOPROTEINASES; GENE-EXPRESSION; MICE; THERAPY; INJURY;
D O I
10.1007/s00441-011-1236-0
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The importance of TNF-alpha signals mediated by tumor necrosis factor receptor type 1 (TNFR1) in inflammation and fibrosis induced by carbon tetrachloride (CCl(4)), and in post-injury liver regeneration including a GFP/CCl(4) model developed as a liver repair model by bone marrow cell (BMC) infusion, was investigated. In mice in which TNFR1 was suppressed by antagonist administration or by knockout, liver fibrosis induced by CCl(4) was significantly decreased. In these mice, intrahepatic macrophage infiltration and TGF-beta 1 expression were reduced and stellate cell activity was decreased; however, expression of MMP-9 was also decreased. With GFP-positive BMC (TNFR1 wildtype, WT) infusion in these mice, fibrosis proliferation, including host endogenous intrahepatic macrophage infiltration, TGF-beta 1 expression and stellate cell activity, increased significantly. There was no significant increase of MMP-9 expression. In this study, TNFR1 in hosts had a promoting effect on CCl(4)-induced hepatotoxicity and fibrosis, whereas BMC infusion in TNFR1 knockout mice enhanced host-derived intrahepatic inflammation and fibrosis proliferation. These findings differed from those in WT recipient mice, in which improvement in inflammation and fibrosis with BMC infusion had previously been reported. TNFR1-mediated signaling might be important to induce the improvement of liver fibrosis by bone marrow cell infusion.
引用
收藏
页码:79 / 88
页数:10
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