Williams R J, Kelly E
Department of Pharmacology, School of Medical Sciences, University of Bristol, England, UK.
J Neurochem. 1993 Sep;61(3):1163-6. doi: 10.1111/j.1471-4159.1993.tb03637.x.
Recent work has shown that chronic ethanol treatment inhibits receptor-stimulated phosphoinositide hydrolysis in NG108-15 cells and that ethanol exerts this effect primarily at the level of the guanine-nucleotide binding protein (G protein). Here we investigated the effects of ethanol exposure on the expression of Gq alpha/11 alpha, two highly homologous G protein alpha-subunits that have been implicated as regulators of phosphoinositidase C. Addition of ethanol (10-200 mM) to the culture medium for 48 h caused a concentration-dependent decrease in the immunologically detectable levels of Gq alpha/11 alpha. A small (approximately 15%) reduction in Gq alpha/11 alpha was observed after only 6 h of exposure to 200 mM ethanol, but membrane levels were reduced by 31% at 48 h. The ethanol-induced loss of Gq alpha/11 alpha was apparently independent of factors present in the foetal calf serum component of the culture medium. These results suggests that the decrease in receptor-mediated phosphoinositide hydrolysis following chronic ethanol treatment of NG108-15 cells may be mediated in part by a reduction in the membrane levels of Gq alpha/11 alpha.
近期研究表明,慢性乙醇处理可抑制NG108 - 15细胞中受体刺激的磷酸肌醇水解,且乙醇主要在鸟嘌呤核苷酸结合蛋白(G蛋白)水平发挥此作用。在此,我们研究了乙醇暴露对Gqα/11α表达的影响,这两种高度同源的G蛋白α亚基被认为是磷脂酶C的调节因子。向培养基中添加乙醇(10 - 200 mM)48小时,导致Gqα/11α的免疫检测水平呈浓度依赖性下降。仅暴露于200 mM乙醇6小时后,Gqα/11α就出现了小幅(约15%)降低,但48小时时膜水平降低了31%。乙醇诱导的Gqα/11α丢失显然与培养基中胎牛血清成分中的因素无关。这些结果表明,慢性乙醇处理NG108 - 15细胞后受体介导的磷酸肌醇水解减少可能部分是由Gqα/11α膜水平降低介导的。