Department of Inner Medicine I, Comprehensive Cancer Center, Institute of Cancer Research, Medical University of Vienna, Vienna, Austria.
PLoS One. 2013 Oct 24;8(10):e76137. doi: 10.1371/journal.pone.0076137. eCollection 2013.
Preceding studies on the mode of action of non-genotoxic hepatocarcinogens (NGCs) have concentrated on alterations induced in hepatocytes (HCs). A potential role of non-parenchymal liver cells (NPCs) in NGC-driven hepatocarcinogenesis has been largely neglected so far. The aim of this study is to characterize NGC-induced alterations in the proteome profiles of HCs as well as NPCs. We chose the prototypic NGC phenobarbital (PB) which was applied to male rats for a period of 14 days. The livers of PB-treated rats were perfused by collagenase and the cell suspensions obtained were subjected to density gradient centrifugation to separate HCs from NPCs. In addition, HCs and NPC isolated from untreated animals were treated with PB in vitro. Proteome profiling was done by CHIP-HPLC and ion trap mass spectrometry. Proteome analyses of the in vivo experiments showed many of the PB effects previously described in HCs by other methods, e.g. induction of phase I and phase II drug metabolising enzymes. In NPCs proteins related to inflammation and immune regulation such as PAI-1 and S100-A10, ADP-ribosyl cyclase 1 and to cell migration such as kinesin-1 heavy chain, myosin regulatory light chain RLC-A and dihydropyrimidinase-related protein 1 were found to be induced, indicating major PB effects on these cells. Remarkably, in vitro treatment of HCs and NPCs with PB hardly reproduced the proteome alterations observed in vivo, indicating differences of NGC induced responses of cells at culture conditions compared to the intact organism. To conclude, the present study clearly demonstrated that PB induces proteome alterations not only in HCs but also in NPCs. Thus, any profound molecular understanding on the mode of action of NGCs has to consider effects on cells of the hepatic mesenchyme.
先前关于非遗传毒性肝癌致癌物 (NGCs) 作用模式的研究集中在肝细胞 (HCs) 中诱导的改变上。迄今为止,非实质肝细胞 (NPCs) 在 NGC 驱动的肝癌发生中的潜在作用在很大程度上被忽视了。本研究旨在表征 HCs 和 NPCs 中 NGC 诱导的蛋白质组谱改变。我们选择了典型的 NGC 苯巴比妥 (PB),将其应用于雄性大鼠 14 天。用胶原酶灌注 PB 处理大鼠的肝脏,获得的细胞悬浮液进行密度梯度离心,以将 HCs 与 NPCs 分离。此外,还将未处理动物的 HCs 和 NPC 与 PB 在体外进行处理。通过 CHIP-HPLC 和离子阱质谱进行蛋白质组分析。体内实验的蛋白质组分析显示了 PB 以前通过其他方法在 HCs 中描述的许多作用,例如诱导 I 相和 II 相药物代谢酶。在 NPCs 中,与炎症和免疫调节相关的蛋白质,如 PAI-1 和 S100-A10、ADP-核糖环化酶 1 以及与细胞迁移相关的蛋白质,如驱动蛋白-1 重链、肌球蛋白调节轻链 RLC-A 和二氢嘧啶酶相关蛋白 1 被发现被诱导,表明 PB 对这些细胞有重大影响。值得注意的是,HCs 和 NPCs 与 PB 体外处理几乎无法复制体内观察到的蛋白质组改变,表明 NGC 诱导的细胞反应在培养条件下与完整生物体不同。总之,本研究清楚地表明,PB 不仅在 HCs 中,而且在 NPCs 中诱导蛋白质组改变。因此,对 NGC 作用模式的任何深入分子理解都必须考虑对肝间质细胞的影响。