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首页> 外文期刊>Comparative Hepatology >Response of sinusoidal mouse liver cells to choline-deficient ethionine-supplemented diet
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Response of sinusoidal mouse liver cells to choline-deficient ethionine-supplemented diet

机译：正弦小鼠肝细胞对补充缺乏胆碱的乙硫氨酸饮食的反应

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Background Proliferation of oval cells, the bipotent precursor cells of the liver, requires impeded proliferation and loss of hepatocytes as well as a specific micro-environment, provided by adjacent sinusoidal cells of liver. Despite their immense importance for triggering the oval cell response, cells of hepatic sinusoids are rarely investigated. To elucidate the response of sinusoidal liver cells we have employed a choline-deficient, ethionine-supplemented (CDE) diet, a common method for inducing an oval cell response in rodent liver. We have utilised selected expression markers commonly used in the past for phenotypic discrimination of oval cells and sinusoidal cells: cytokeratin, E-cadherin and M2-pyruvate kinase for oval cells; and glial fibrillary acidic protein (GFAP) was used for hepatic stellate cells (HSCs). Results CDE diet leads to an activation of all cells of the hepatic sinusoid in the mouse liver. Beside oval cells, also HSCs and Kupffer cells proliferate. The entire fraction of proliferating cells in mouse liver as well as endothelial cells and cholangiocytes express M2-pyruvate kinase. Concomitantly, GFAP, long considered a unique marker of quiescent HSCs was upregulated in activated HSCs and expressed also in cholangiocytes and oval cells. Conclusions Our results point to an important role of all types of sinusoidal cells in regeneration from CDE induced liver damage and call for utmost caution in using traditional marker for identifying specific cell types. Thus, M2-pyruvate kinase should no longer be used for estimating the oval cell response in mouse liver. CDE diet leads to activation of GFAP positive HSCs in the pericentral zone of liver lobulus. In the periportal zone the detection of GFAP in biliary cells and oval cells, calls other cell types as progenitors of hepatocytes into question under CDE diet conditions.
机译：背景技术卵圆形细胞（肝脏的双能前体细胞）的增殖需要阻止肝细胞的增殖和丧失，以及相邻肝正弦细胞所提供的特定微环境。尽管它们对于触发卵圆细胞反应具有极为重要的意义，但很少研究肝窦的细胞。为了阐明正弦肝细胞的反应，我们采用了胆碱缺乏，补充乙硫氨酸的饮食（CDE），这是在啮齿动物肝脏中诱导卵圆细胞反应的常用方法。我们利用了过去通常用于卵形细胞和正弦细胞表型识别的选定表达标记：卵圆细胞的细胞角蛋白，E-钙粘着蛋白和M2-丙酮酸激酶。胶质纤维酸性蛋白（GFAP）用于肝星状细胞（HSC）。结果CDE饮食导致小鼠肝脏中肝窦的所有细胞均被激活。除了卵圆形细胞外，HSC和库普弗细胞也会增殖。小鼠肝脏中的增殖细胞的全部部分以及内皮细胞和胆管细胞都表达M2丙酮酸激酶。随之而来的是，长期以来被认为是静态HSC独特标志物的GFAP在活化的HSC中上调，并在胆管细胞和卵圆形细胞中表达。结论我们的结果表明，所有类型的正弦细胞在CDE诱导的肝损伤再生中都具有重要作用，因此在使用传统标记物识别特定细胞类型时要格外谨慎。因此，M2-丙酮酸激酶不应再用于估计小鼠肝脏中的卵圆细胞反应。 CDE饮食可导致肝小叶中央区的GFAP阳性HSC活化。在肝周区，胆汁细胞和卵圆形细胞中GFAP的检测使其他类型的细胞成为肝细胞的祖细胞，这在CDE饮食条件下受到质疑。

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