Yamaguchi T, Fukase M, Fujita T
Department of Medicine, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1988 Dec 30;157(3):908-13. doi: 10.1016/s0006-291x(88)80960-4.
To clarify the possible role of protein kinase C in the control of parathyroid hormone (PTH)-degrading activity (PTHDA) in a PTH-responsive opossum kidney (OK) cell line, we investigated the effects of protein kinase C activators, 12-O-tetradecanoyl phorbol 13-acetate (TPA), 1-oleoyl-2-acetyl-glycerol (OAG), and 4 beta-phorbol 12, 13-didecanoate (4 beta-PDD). TPA, OAG, and 4 beta-PDD enhanced PTHDA in a dose-dependent fashion (10-50 ng/ml, 10-100 microgram/ml, and 10-50 nM, respectively), whereas 4 alpha-PDD, a non-activator of protein kinase C, did not affect it. HPLC analysis of TPA-treated samples revealed increase of all immunoreactive PTH fragments produced by OK cells. These findings suggested that activation of protein kinase C in OK cells would augment PTHDA in the cells.
为了阐明蛋白激酶C在调控甲状旁腺激素（PTH）降解活性（PTHDA）方面可能发挥的作用，我们以一种对PTH有反应的负鼠肾（OK）细胞系展开研究，考察了蛋白激酶C激活剂12 - O - 十四烷酰佛波醇13 - 乙酸酯（TPA）、1 - 油酰基 - 2 - 乙酰甘油（OAG）和4β - 佛波醇12,13 - 二癸酸酯（4β - PDD）的作用。TPA、OAG和4β - PDD以剂量依赖方式增强PTHDA（分别为10 - 50 ng/ml、10 - 100 μg/ml和10 - 50 nM），而蛋白激酶C的非激活剂4α - PDD则无此作用。对TPA处理样本的高效液相色谱分析显示，OK细胞产生的所有免疫反应性PTH片段均增加。这些发现表明，OK细胞中蛋白激酶C的激活会增强细胞内的PTHDA。
