EMT对纤维化无贡献,何如肿瘤?  

No contribution to liver fibrosis,but possible carcinogenesis?

作　　者：张大伟[1] 边惠洁[1] 

机构地区：[1]第四军医大学基础部细胞工程中心细胞生物学教研室,陕西西安710032

出　　处：《医学争鸣》2011年第2期26-30,共5页Negative

摘　　要：2010年3月在《肝脏病学》(Hepatology)上刊登了一篇题为"在小鼠肝纤维化过程中肝细胞并没有发生表皮间质细胞转化现象"的文章。经过仔细研读这篇文献,我们发现作者的试验结果中体内试验与体外试验结果不一致,采取的纤维化小鼠动物模型单一,并且间质细胞分子标志物α-SMA染色阴性,这一结果与我们前期研究结果相反。针对以上三点问题我们提出疑问和自己的见解,得到了编辑的肯定,撰写的Correspondence在2010年4月的《Hepatology》杂志上发表。An article entitled ＂Hepatocytes do not undergo epithelial-mesenchymal transition in liver fibrosis in mice＂ provided evidences that hepatocytes in vivo neither express mesenchymal markers nor exhibit a morphological change, which strongly challenges the earlier concept that hepatocytes in vivo acquire a mesenchymal phenotype through epithelial-mesenchymal transition （EMT） to produce the extra cellular matrix leading to liver fibrosis. Based on our experiments and others＇ previous studies, several issues need to be further discussed. Firstly, we do not know whether the currently prevalent liver fibrosis models truly reflect the changes of the hepatocytes in liver injury. Therefore, the existence of EMT of hepatocytes in liver fibrosis still seems to be an open question. Secondly, EMT is reported to be involved in hepatocarcinogenesis. We detected ct-SMA expression in the cytoplasm of hyperplastic hepatocytes and in the perisinusoidal space by immunohistochemistry in carbon tetrachloride-induced mouse liver fibrosis sections, implying EMT as an outcome of anti-apoptosis in carcinogenesis. Finally, due to the insufficient evidences from literatures and limitation of the study as mentioned by the authors, more detailed studies with translational medicine methodology need to verify the existence of EMT of hepatocytes followed by investigation of its related role in liver diseases including liver fibrosis and hepatocellular carcinoma development.

关 键 词：表皮间质细胞转化 肝癌 肝纤维化 

分 类 号：R657.34[医药卫生—外科学]