Hepatic gene expression in hepatocyte-specific Pten deficient mice showing steatohepatitis without ethanol challenge
Hepatic gene expression in hepatocyte-specific Pten deficient mice showing steatohepatitis without ethanol challenge
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DOI：
10.1016/j.hepres.2006.01.003
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发表时间：
2006-04-01
影响因子：
4.2
通讯作者：
Watanabe, S
中科院分区：
文献类型：
--
作者：
Sato, W;Horie, Y;Watanabe, S
肝细胞特异性Pten缺陷（Pten KO）小鼠在组织学上具有与人NASH几乎相同的肝脏病变，并且被认为代表一些有限的NASH患者。我们使用DNA微阵列技术分析了10- 35周龄Pten KO小鼠肝细胞的全面基因表达，以寻找与人类NASH发生和加重相关的候选基因。Spp 1、Vnn 1、Itga 6、Abcd 2、Auh、Acox 1、Pdk 4、Cpt 1a、Lcn 2、Igfbp 2、Gstm 6、Socs 3、Tgm 2和Aldh 9a 1被认为是与炎症相关的候选基因。Spp 1、Ctgf和Cyp 2c 39是纤维化的候选基因，Cidec和Spp 1是癌变的候选基因。为了证实这些基因对某些人类NASH的病因学有贡献，需要使用人类肝脏样本进行进一步研究。(c)2006爱思唯尔爱尔兰有限公司保留所有权利。
Hepatocyte-specific Pten deficient (Pten KO) mice possess almost the same hepatic lesions histologically as human NASH and are thought to represent some limited NASH patients. We analyzed a comprehensive gene expression of hepatocytes derived from 10- to 35-week-old Pten KO mice using the DNA microarray technology to find out the candidate genes related to development and aggravation of human NASH. Spp1, Vnn1, Itga6, Abcd2, Auh, Acox1, Pdk4, Cpt1a, Lcn2, Igfbp2, Gstm6, Socs3, Tgm2, and Aldh9a1 were regarded as the candidate genes related to inflammation. The candidate genes of fibrosis were Spp1, Ctgf, and Cyp2c39 and moreover Cidec and Spp1 were regarded as the candidate genes of carcinogenesis. To confirm that these genes contribute to the etiology of some human NASH, further investigations using human liver samples are needed. (c) 2006 Elsevier Ireland Ltd. All rights reserved.