Galectin-3 regulates myofibroblast activation and hepatic fibrosis

Henderson NC; Mackinnon AC; Farnworth SL; Poirier F; Russo FP; Iredale JP; Haslett C; Simpson KJ; Sethi T

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Galectin-3 regulates myofibroblast activation and hepatic fibrosis

机译：Galectin-3调节成纤维细胞活化和肝纤维化

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Central to fibrogenesis and the scarring of organs is the activation of fibroblasts into matrix-secreting myofibroblasts. We demonstrate that Galectin-3 expression is up-regulated in established human fibrotic liver disease and is temporally and spatially related to the induction and resolution of experimental hepatic fibrosis. Disruption of the Galectin-3 gene blocks myofibroblast activation and procollagen (1) expression in vitro and in vivo, markedly attenuating liver fibrosis. Addition of exogenous recombinant Galectin-3 in vitro reversed this abnormality. The reduction in hepatic fibrosis observed in the Galectin-3(-/-) mouse occurred despite equivalent liver injury and inflammation, and similar tissue expression of TGF-beta. TGF-beta failed to transactivate Galectin-3(-/-) hepatic stellate cells, in contrast with WT hepatic stellate cells; however, TGF-beta-stimulated Smad-2 and -3 activation was equivalent. These data suggest that Galectin-3 is required for TGF-beta mediated myofibroblast activation and matrix production. Finally, in vivo siRNA knockdown of Galectin-3 inhibited myofibroblast activation after hepatic injury and may therefore provide an alternative therapeutic approach to the prevention and treatment of liver fibrosis.

机译：成纤维和器官瘢痕形成的关键是成纤维细胞活化为分泌基质的成肌纤维细胞。我们证明Galectin-3的表达在已建立的人类纤维化肝病中被上调，并且在时间和空间上与实验性肝纤维化的诱导和分离有关。 Galectin-3基因的破坏在体外和体内阻断了肌成纤维细胞的活化和原胶原（1）的表达，从而明显减轻了肝纤维化。体外添加外源重组Galectin-3可逆转这种异常。尽管肝损伤和炎症等效，并且TGF-beta的组织表达相似，但在Galectin-3（-/-）小鼠中观察到肝纤维化的减少。与野生型肝星状细胞相反，TGF-β无法激活Galectin-3（-/-）肝星状细胞。然而，TGF-β刺激的Smad-2和-3激活是等效的。这些数据表明Galectin-3是TGF-β介导的成纤维细胞活化和基质产生所必需的。最后，Galectin-3的体内siRNA敲低抑制了肝损伤后肌成纤维细胞的活化，因此可以为肝纤维化的预防和治疗提供另一种治疗方法。

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来源
《Proceedings of the National Academy of Sciences of the United States of America》 |2006年第13期|p. 5060-5065|共6页
作者
Henderson NC; Mackinnon AC; Farnworth SL; Poirier F; Russo FP; Iredale JP; Haslett C; Simpson KJ; Sethi T;
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作者单位

Univ Edinburgh, Queens Med Res Inst, Ctr Inflammat Res, Edinburgh EH16 4SA, Midlothian, Scotland;

Inst Jacques Monod, Lab Genet & Dev Mammiferes, F-75251 Paris 05, France;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
关键词
hepatic stellate cell; liver; small interfering RNA; TGF-beta; CARBOHYDRATE-BINDING PROTEIN; BREAST EPITHELIAL-CELLS; STELLATE CELLS; PULMONARY-FIBROSIS; SIGNALING PATHWAYS; LIVER FIBROSIS; ANIMAL LECTINS; BETA; EXPRESSION; GROWTH;

机译：肝星状细胞;肝脏;小干扰RNA;TGF-β;与碳水化合物结合的蛋白;乳腺上皮细胞;星状细胞;肺纤维化;信号通路;肝纤维化;动物血凝素;BETA;表达;生长;

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机译：抑制组氨酸丰富的钙结合蛋白（HRC）通过抑制肝星状细胞的激活抑制肝纤维化抑制组氨酸丰富的组氨酸钙结合蛋白（HRC）通过抑制肝星状细胞的抑制肝纤维化丰富的钙结合蛋白（HRC）通过抑制肝星状细胞的活化来抑制肝纤维化
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机译：11Beta-羟类脱氢酶-1缺乏或抑制增强了鼠肝纤维化的肝肌纤维细胞活化
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5. Intracellular signaling pathways regulating hepatic apolipoprotein B100 production: Role of mitogen -activated protein kinases (MAPKs) and inhibitor of NFkappaB kinase (IKK)-NFkappaB. [D] . Tsai, Julie Wen-chia. 2009

机译：调节肝载脂蛋白B100产生的细胞内信号传导途径：促分裂原活化蛋白激酶（MAPK）和NFkappBB激酶（IKK）-NFkappaB抑制剂的作用。
6. Galectin-3 regulates myofibroblast activation and hepatic fibrosis [O] . Neil C. Henderson, Alison C. Mackinnon, Sarah L. Farnworth, 2006

机译：Galectin-3调节成纤维细胞活化和肝纤维化
7. Galectin-3 regulates myofibroblast activation and hepatic fibrosis [O] . Henderson, Neil C., Mackinnon, Alison C., Farnworth, Sarah L., 2006

机译：Galectin-3调节成纤维细胞活化和肝纤维化

Galectin-3 regulates myofibroblast activation and hepatic fibrosis

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