Michalke M, Cariers A, Schliess F, Häussinger D
Department of Gastroenterology, Hepatology and Infectiology, Heinrich-Heine-University, Moorenstr. 5, D-40225, D]usseldorf, Germany.
FEBS Lett. 2000 Jan 7;465(1):64-8. doi: 10.1016/s0014-5793(99)01719-6.
The influence of anisoosmolarity on NF-kappaB binding activity was studied in H4IIE rat hepatoma cells. Hypoosmolarity induced a sustained NF-kappaB binding activity whereas the hyperosmotic NF-kappaB response was only minor. Hypoosmotic NF-kappaB activation was accompanied by degradation of the inhibitory IkappaB-alpha. Protein kinase C, PI(3)-kinase, reactive oxygen intermediates and the proteasome apparently participate in mediating the hypoosmotic effect on NF-kappaB. Hypoosmolarity plus PMA induced, amplified and prolonged IkappaB-alpha degradation and NF-kappaB binding activity. Transforming growth factor beta-induced apoptosis was diminished by hypoosmolarity. However, this anti-apoptotic effect was probably not related to NF-kappaB activation.
在H4IIE大鼠肝癌细胞中研究了非等渗对NF-κB结合活性的影响。低渗诱导了持续的NF-κB结合活性,而高渗时NF-κB的反应则很轻微。低渗诱导的NF-κB激活伴随着抑制性IκB-α的降解。蛋白激酶C、磷脂酰肌醇-3激酶、活性氧中间体和蛋白酶体显然参与介导低渗对NF-κB的作用。低渗加佛波酯诱导、放大并延长了IκB-α的降解和NF-κB结合活性。低渗可减少转化生长因子β诱导的细胞凋亡。然而,这种抗凋亡作用可能与NF-κB激活无关。