Isomura H, Sawada N, Nakajima Y, Sakamoto H, Ikeda T, Kojima T, Enomoto K, Mori M
Department of Pathology, Sapporo Medical College, Japan.
J Cell Physiol. 1993 Feb;154(2):329-32. doi: 10.1002/jcp.1041540216.
We examined expression of the c-myc oncogene in isolated perfused livers to elucidate the mechanisms involved in triggering the proliferation of hepatocytes after partial hepatectomy (PH). During perfusion with a 1:1 mixture of Dulbecco's modified Eagle's medium and the oxygen transport fluid FC-43, rat livers were two-thirds resected (PH), and further perfused for 1 1/2 hours at the physiological portal flow throughout the perfusion. Expression of c-myc in the perfused livers with PH(+) was ten times higher than in those with PH(-). Furthermore, expression of c-myc in the PH(-) livers perfused with a threefold volume of the physiological portal flow was 5-10 times higher than that in the livers perfused with the physiological portal flow. The perfusates that passed through the livers did not induce DNA synthesis of primary cultured hepatocytes. These results suggest that an increase in the portal flow volume may act as a trigger for hepatocyte proliferation after PH.
我们检测了分离灌注肝脏中c-myc癌基因的表达，以阐明部分肝切除（PH）后触发肝细胞增殖的相关机制。在用杜氏改良伊格尔培养基和氧转运液FC-43按1:1混合的溶液进行灌注期间，将大鼠肝脏切除三分之二（PH），并在整个灌注过程中以生理门静脉血流量进一步灌注1.5小时。PH（+）灌注肝脏中c-myc的表达比PH（-）灌注肝脏中的高10倍。此外，用三倍生理门静脉血流量灌注的PH（-）肝脏中c-myc的表达比用生理门静脉血流量灌注的肝脏中的高5至10倍。流经肝脏的灌注液未诱导原代培养肝细胞的DNA合成。这些结果表明，门静脉血流量的增加可能是PH后肝细胞增殖的触发因素。
