Sariban-Sohraby S, Burg M, Wiesmann W P, Chiang P K, Johnson J P
Science. 1984 Aug 17;225(4663):745-6. doi: 10.1126/science.6463652.
When isolated apical membrane vesicles prepared from cultured A6 epithelia were incubated in vitro with the methyl donor S-adenosylmethionine, the control rate of amiloride-inhibitable sodium transport was doubled. The methylation inhibitors 3-deazaadenosine and S-adenosyl homocysteine returned the S-adenosyl-methionine-stimulated sodium transport to control levels. Neither these agents nor adenosine affected sodium transport into control vesicles. In vesicles incubated with S-adenosyl-[3H-methyl]methionine, both membrane phospholipids and proteins were labeled, and this labeling was inhibited by deazaadenosine. In vesicles prepared from A6 cells treated with aldosterone, sodium transport was twice the control value and S-adenosylmethionine did not cause any further stimulation of transport. In those vesicles, both lipid and protein methylation were increased. These results suggest that methylation, which increases the rate of amiloride-sensitive sodium transport is involved in the action of aldosterone at the apical membrane level in epithelia.
当用甲基供体S-腺苷甲硫氨酸在体外孵育从培养的A6上皮细胞制备的分离的顶端膜囊泡时，氨氯地平可抑制的钠转运的对照速率增加了一倍。甲基化抑制剂3-脱氮腺苷和S-腺苷同型半胱氨酸使S-腺苷甲硫氨酸刺激的钠转运恢复到对照水平。这些试剂和腺苷均不影响钠转运进入对照囊泡。在用S-腺苷-[3H-甲基]甲硫氨酸孵育的囊泡中，膜磷脂和蛋白质均被标记，并且这种标记被脱氮腺苷抑制。在用醛固酮处理的A6细胞制备的囊泡中，钠转运是对照值的两倍，并且S-腺苷甲硫氨酸不会引起转运的任何进一步刺激。在那些囊泡中，脂质和蛋白质甲基化均增加。这些结果表明，增加氨氯地平敏感的钠转运速率的甲基化参与了醛固酮在上皮细胞顶端膜水平的作用。
