Schliess Freimut, Schäfer Christine, vom Dahl Stephan, Fischer Richard, Lordnejad Mohammad R, Häussinger Dieter
Clinic for Gastroenterology, Hepatology and Infectiology, Heinrich-Heine-University, D-40225 Düsseldorf, Germany.
Arch Biochem Biophys. 2002 May 15;401(2):187-97. doi: 10.1016/S0003-9861(02)00047-4.
The expression of sodium potassium chloride cotransporter 1 (NKCC1) was studied in different liver cell types. NKCC1 was found in rat liver parenchymal and sinusoidal endothelial cells and in human HuH-7 hepatoma cells. NKCC1 expression in rat hepatic stellate cells increased during culture-induced transformation in the myofibroblast-like phenotype. NKCC1 inhibition by bumetanide increased alpha(1)-smooth muscle actin expression in 2-day-cultured hepatic stellate cells but was without effect on basal and platelet-derived-growth-factor-induced proliferation of the 14-day-old cells. In perfused rat liver the NKCC1 made a major contribution to volume-regulatory K(+) uptake induced by hyperosmolarity. Long-term hyperosmotic treatment of HuH-7 cells by elevation of extracellular NaCl or raffinose concentration but not hyperosmotic urea or mannitol profoundly induced NKCC1 mRNA and protein expression. This was antagonized by the compatible organic osmolytes betaine or taurine. The data suggest a role of NKCC1 in stellate cell transformation, hepatic volume regulation, and long-term adaption to dehydrating conditions.
研究了钠钾氯共转运体1（NKCC1）在不同肝细胞类型中的表达。在大鼠肝实质细胞和窦状内皮细胞以及人HuH-7肝癌细胞中发现了NKCC1。在培养诱导的肌成纤维细胞样表型转化过程中，大鼠肝星状细胞中NKCC1的表达增加。布美他尼抑制NKCC1可增加培养2天的肝星状细胞中α(1)-平滑肌肌动蛋白的表达，但对14天龄细胞的基础增殖和血小板衍生生长因子诱导的增殖没有影响。在灌注大鼠肝脏中，NKCC1对高渗诱导的容量调节性钾摄取起主要作用。通过提高细胞外氯化钠或棉子糖浓度对HuH-7细胞进行长期高渗处理，但高渗尿素或甘露醇则不会，可显著诱导NKCC1 mRNA和蛋白表达。这被相容性有机渗透剂甜菜碱或牛磺酸所拮抗。数据表明NKCC1在星状细胞转化、肝脏容量调节和对脱水条件的长期适应中起作用。
