Lipopolysaccharide induces the differentiation of hepatic progenitor cells into myofibroblasts via activation of the Hedgehog signaling pathway
Lipopolysaccharide induces the differentiation of hepatic progenitor cells into myofibroblasts via activation of the Hedgehog signaling pathway
复制标题
脂多糖通过激活 Hedgehog 信号通路诱导肝祖细胞分化为肌成纤维细胞
DOI：
10.1080/15384101.2017.1325976
复制
发表时间：
2017-05
期刊：
影响因子：
4.3
通讯作者：
Wei Li-xin
中科院分区：
文献类型：
--
作者：
Pan Xiao-rong;Jing Ying-ying;Liu Wen-ting;Han Zhi-peng;Li Rong;Yang Yang;Zhu Jing-ni;Li Xiao-yong;Li Pei-pei;Wei Li-xin
正常情况下，肝损伤过程中肝祖细胞（HPCs）被激活并分化为肝细胞或胆管细胞，修复肝损伤。然而，HPCs的异常分化是否发生在异常条件下仍存在争议。脂多糖（LPS），微环境的一个组成部分，促进肝纤维化。在本研究中，HPCs促进了四氯化碳（CCl4）治疗后大鼠的肝纤维化。同时，门静脉内LPS水平升高，在HPCs的命运中起主要作用。在体外实验中，LPS抑制HPCs的肝胆分化。同时，与LPS共培养2周的HPCs有向肌成纤维细胞（MFs）分化的趋势。因此，我们得出结论，LPS促进HPCs异常分化为MFs作为第三种类型的后代。这项研究为HPCs在微环境中的新分化命运提供了见解，并可能因此导致HPCs用于肝纤维化治疗方法的发展。
Abstract Normally, hepatic progenitor cells (HPCs) are activated and differentiate into hepatocytes or bile ductular cells to repair liver damage during liver injury. However, it remains controversial whether the abnormal differentiation of HPCs occurs under abnormal conditions. Lipopolysaccharide (LPS), a component of the microenvironment, promotes liver fibrosis. In the present study, HPCs promoted liver fibrosis in rats following carbon tetrachloride (CCl4) treatment. Meanwhile, the LPS level in the portal vein was elevated and played a primary role in the fate of HPCs. In vitro, LPS inhibited the hepatobiliary differentiation of HPCs. Concurrently, HPCs co-cultured with LPS for 2 weeks showed a tendency to differentiate into myofibroblasts (MFs). Thus, we conclude that LPS promotes the aberrant differentiation of HPCs into MFs as a third type of descendant. This study provides insight into a novel differentiation fate of HPCs in their microenvironment, and could thus lead to the development of HPCs for treatment methods in liver fibrosis.
登录
查看更多内容
影响因子：
5.6
作者：
Carpino G;Renzi A;Onori P;Gaudio E
通讯作者：
Gaudio E
影响因子：
--
作者：
Ceccarelli S;Panera N;Mina M;Gnani D;De Stefanis C;Crudele A;Rychlicki C;Petrini S;Bruscalupi G;Agostinelli L;Stronati L;Cucchiara S;Musso G;Furlanello C;Svegliati-Baroni G;Nobili V;Alisi A
通讯作者：
Alisi A
影响因子：
4.6
作者：
Chang LY;Li Y;Kaplan DE
通讯作者：
Kaplan DE
影响因子：
5.9
作者：
Sekiya, Sayaka;Miura, Shizuka;Matsuda-Ito, Kanae;Suzuki, Atsushi
通讯作者：
Suzuki, Atsushi
影响因子：
13.5
作者：
Clouston, AD;Powell, EE;Jonsson, JR
通讯作者：
Jonsson, JR