Shi Lijun, Li Guozhong, Wang Jinghua, Sun Bo, Yang Liming, Wang Guangyou, Wang Dandan, Mu Lili, Chen Hui, Jin Lianhong, Kostulas Nikolaos, Li Hulun
Department of Gastroenterology, The First Affiliated Clinic College of Harbin Medical University, Heilongjiang, China.
Dig Dis Sci. 2008 Nov;53(11):2969-74. doi: 10.1007/s10620-008-0227-9. Epub 2008 Mar 20.
Liver cirrhosis is characterized by hepatic dysfunction, with extensive accumulation of fibrous tissue in the liver. Hepatic stellate cells (HSCs) are the major source of fibrillar matrix proteins and play an important role in the progress of liver cirrhosis. In our study, the growth of HSCs is inhibited by bone marrow stromal cells (BMSCs). The inhibition is irreversible and is followed by apoptosis. The effect of BMSCs on the apoptosis of HSCs is possibly via the JNK pathway activated by nerve growth factor (NGF) and hepatocyte growth factor (HGF) secreted by BMSCs. Meanwhile, the apoptosis effect is enhanced by transforming growth factor-beta blocking.
肝硬化的特征是肝功能障碍,肝脏中纤维组织广泛积聚。肝星状细胞(HSCs)是纤维状基质蛋白的主要来源,在肝硬化进展中起重要作用。在我们的研究中,骨髓基质细胞(BMSCs)抑制了HSCs的生长。这种抑制是不可逆的,随后会发生凋亡。BMSCs对HSCs凋亡的作用可能是通过由BMSCs分泌的神经生长因子(NGF)和肝细胞生长因子(HGF)激活的JNK途径实现的。同时,转化生长因子-β阻断可增强凋亡作用。