Yamazaki Taisuke, Wakai Mariko, Enosawa Shin, Tokiwa Takayoshi
Department of Liver Cell Biology, Kohno Clinical Medicine Research Institute, Tokyo, Japan.
Division for Advanced Medical Sciences, National Center for Child Health and Development, Tokyo, Japan.
In Vitro Cell Dev Biol Anim. 2017 Jun;53(6):564-573. doi: 10.1007/s11626-017-0144-3. Epub 2017 Mar 31.
Biliary atresia (BA) is a rare and serious liver disease in newborn infants. Previously, we reported that non-parenchymal cell (NPC) fractions from cirrhotic liver of BA may contain hepatic stem/progenitor cells in primary culture of NPC fractions. In this study, NPC fractions were subjected to primary or passage culture and found that clusters of hepatocyte-like cells appear even without adding hepatocyte growth factor (HGF) to the culture medium, but not in their passage culture used as a control. Based on these findings, conditioned media (CMs) were collected and soluble factors in the CMs were analyzed in order to elucidate the mechanism of the appearance of hepatocyte-like cells or their clusters. A large amount of active HGF consisting of α and β chains was detected in CMs derived from primary culture, but not in CMs from passage culture, as determined by western blot analysis, bone morphogenetic protein (BMP)-4, oncostatin M (OSM), and transforming growth factor (TGF)-β1 were not detected in any of the CMs. The number of hepatocyte-like cells in primary culture tended to decrease following treatment with the HGF receptor c-Met inhibitor, SU11274 in a dose-dependent manner. Furthermore, the clusters of hepatocyte-like cells tended to increase in size and number when freshly isolated NPC fractions were cultured in the presence of 10% of CMs collected after 3-4 wk of primary culture. In conclusion, these findings indicate that CMs derived from primary culture of NPC fractions of BA liver contain a large amount of active HGF, which may activate hepatic stem/progenitor cells and promote the appearance of hepatocyte-like cells or their clusters through HGF/c-Met signaling. The present study would lead to cell therapy using the patient's own cells for the treatment of BA.
胆道闭锁(BA)是一种发生于新生儿的罕见且严重的肝脏疾病。此前,我们报道过,在对BA肝硬化肝脏的非实质细胞(NPC)组分进行原代培养时,其可能含有肝干细胞/祖细胞。在本研究中,对NPC组分进行原代或传代培养,发现即使在培养基中不添加肝细胞生长因子(HGF),也会出现肝细胞样细胞簇,但作为对照的传代培养中则未出现。基于这些发现,收集了条件培养基(CMs)并分析了其中的可溶性因子,以阐明肝细胞样细胞或其细胞簇出现的机制。通过蛋白质印迹分析确定,在原代培养衍生的CMs中检测到大量由α链和β链组成的活性HGF,但传代培养的CMs中未检测到;在任何CMs中均未检测到骨形态发生蛋白(BMP)-4、制瘤素M(OSM)和转化生长因子(TGF)-β1。用HGF受体c-Met抑制剂SU11274处理后,原代培养中肝细胞样细胞的数量呈剂量依赖性减少。此外,当在原代培养3 - 4周后收集的10%的CMs存在的情况下培养新鲜分离的NPC组分时,肝细胞样细胞簇的大小和数量趋于增加。总之,这些发现表明,BA肝脏NPC组分原代培养衍生的CMs含有大量活性HGF,其可能通过HGF/c-Met信号激活肝干细胞/祖细胞并促进肝细胞样细胞或其细胞簇的出现。本研究将导向使用患者自身细胞治疗BA的细胞疗法。