Häussinger D, Stoll B, vom Dahl S, Theodoropoulos P A, Markogiannakis E, Gravanis A, Lang F, Stournaras C
Medizinische Universitätsklinik, Freiburg, Germany.
Biochem Cell Biol. 1994 Jan-Feb;72(1-2):12-9. doi: 10.1139/o94-003.
Incubation of isolated rat hepatocytes under conditions known to induce cell swelling caused several alterations in microtubule physiology. As shown by immunofluorescence microscopy experiments in the absence and presence of triethyllead or colchicine (two well-established microtubule inhibitors), an apparent stabilization of the microtubule network became evident in hepatocytes exposed to hypotonic (190 mosmol/L) conditions. A similar stabilizing effect was also observed upon cell swelling induced by addition of insulin (100 nmol/L) or glutamine (10 mmol/L). The differential microtubule stabilities were not attributed to a differential incorporation of the antimicrotubular agents into hepatocytes as shown by [3H]colchicine-uptake experiments. The swelling-induced alterations of microtubules may contribute to the swelling-induced changes of liver cell function: in perfused rat liver it was found that the established inhibitory effect of hypotonic cell swelling on hepatic proteolysis was largely abolished in presence of colchicine. Tubulin mRNA levels increased by 1.9-, 2.1- and 2.7-fold in isolated hepatocytes being exposed for 120 min to hypotonic medium, insulin, or glutamine, respectively. The results suggest an involvement of microtubular structures in the regulation of liver metabolism in response to alterations of the cellular hydration state.
在已知会诱导细胞肿胀的条件下培养分离的大鼠肝细胞，会导致微管生理学发生多种改变。如在不存在和存在三乙基铅或秋水仙碱（两种公认的微管抑制剂）的情况下进行的免疫荧光显微镜实验所示，在暴露于低渗（190 mosmol/L）条件的肝细胞中，微管网络明显稳定。在添加胰岛素（100 nmol/L）或谷氨酰胺（10 mmol/L）诱导细胞肿胀时也观察到了类似的稳定作用。如[3H]秋水仙碱摄取实验所示，微管稳定性的差异并非归因于抗微管药物进入肝细胞的差异。微管肿胀诱导的改变可能导致肝细胞功能的肿胀诱导变化：在灌注大鼠肝脏中发现，在存在秋水仙碱的情况下，低渗细胞肿胀对肝脏蛋白水解的既定抑制作用在很大程度上被消除。在分别暴露于低渗培养基、胰岛素或谷氨酰胺120分钟的分离肝细胞中，微管蛋白mRNA水平分别增加了1.9倍、2.1倍和2.7倍。结果表明微管结构参与了肝脏代谢对细胞水合状态改变的调节。
