Souza G M, Klein C, Maia J C, Da Silva A M
Departamento de Bioquímica, Universidade de São Paulo, Brazil.
Cell Signal. 1994 Nov;6(8):883-95. doi: 10.1016/0898-6568(94)90021-3.
The mechanism by which high concentrations of cAMP selectively destabilize the gp80 mRNA in Dictyostelium discoideum was investigated. This treatment which leads to down-regulation of the cAMP receptor was also found to cause an increase in calcium uptake. Given this observation, we sought a role for calcium as a second messenger in the degradation of the gp80 mRNA. Changes in the mRNA levels were examined after treating cells with compounds known to alter their intracellular Ca2+ concentrations. This included the use of A23187, Ca2+, 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate HC1 (TMB-8), LiCl and 8-p-chlorophenylthioadenosine 3',5'-cyclic monophosphate (ClPhS-Ado-3':5'-P). The sum of the data suggest that it is the cAMP-induced influx of Ca2+ across the plasma membrane, as apposed to a cAMP-mediated release of Ca2+ from intracellular stores, that initiates gp80 mRNA degradation. Treatment of cells with Concanavalin A (ConA) to induce cAMP receptor down-regulation, also causes a reduction in gp80 mRNA levels and an increase in calcium uptake.
研究了高浓度环磷酸腺苷（cAMP）选择性地使盘基网柄菌中gp80信使核糖核酸（mRNA）不稳定的机制。这种导致cAMP受体下调的处理方法还被发现会使钙摄取增加。基于这一观察结果，我们探寻钙作为第二信使在gp80 mRNA降解中的作用。在用已知可改变细胞内钙离子（Ca2+）浓度的化合物处理细胞后，检测了mRNA水平的变化。这包括使用A23187、Ca2+、8-（N，N-二乙氨基）辛基-3,4,5-三甲氧基苯甲酸盐酸盐（TMB-8）、氯化锂（LiCl）和8-对氯苯硫基腺苷3',5'-环一磷酸（ClPhS-Ado-3':5'-P）。所有数据表明，是cAMP诱导的Ca2+跨质膜内流，而不是cAMP介导的细胞内钙库释放Ca2+，启动了gp80 mRNA的降解。用刀豆球蛋白A（ConA）处理细胞以诱导cAMP受体下调，也会导致gp80 mRNA水平降低和钙摄取增加。
