Doherty P, Walsh F S
J Neurochem. 1987 Aug;49(2):610-6. doi: 10.1111/j.1471-4159.1987.tb02907.x.
The effects of nerve growth factor (NGF) and cholera toxin on the expression of the Thy-1 glycoprotein were examined in cultures of naive and primed PC12 cells using an enzyme-linked immunoadsorbent assay (ELISA). With primed PC12 cells, NGF induced a rapid increase in Thy-1 expression over a time course similar to that of neurite regeneration, with half-maximal and maximal increases apparent at 0.6 and 6 ng/ml NGF. Cholera toxin and dibutyryl cyclic AMP, but not B-cholera toxin or antibodies to the toxin receptor, were found to inhibit NGF-induced increases in Thy-1. Morphological differentiation of naive PC12 cells induced by NGF, but not cholera toxin, was also associated with increased expression of Thy-1. Despite showing a synergistic effect on morphological differentiation, cholera toxin was again found to inhibit NGF-induced increases in Thy-1 expression in cultures of naive PC12 cells. These data suggest that agents that interact directly or indirectly with adenylate cyclase may regulate the responsiveness of PC12 cells to NGF, and as such modulate the expression of the Thy-1 glycoprotein.
利用酶联免疫吸附测定法（ELISA），在未致敏和已致敏的PC12细胞培养物中检测了神经生长因子（NGF）和霍乱毒素对Thy-1糖蛋白表达的影响。对于已致敏的PC12细胞，NGF在类似于神经突再生的时间进程中诱导Thy-1表达迅速增加，在0.6和6 ng/ml NGF时分别出现半数最大增加和最大增加。发现霍乱毒素和二丁酰环磷腺苷（dibutyryl cyclic AMP），而非B型霍乱毒素或毒素受体抗体，可抑制NGF诱导的Thy-1增加。NGF诱导的未致敏PC12细胞的形态分化（而非霍乱毒素诱导的）也与Thy-1表达增加有关。尽管霍乱毒素对形态分化显示出协同作用，但再次发现其可抑制未致敏PC12细胞培养物中NGF诱导的Thy-1表达增加。这些数据表明，直接或间接与腺苷酸环化酶相互作用的试剂可能调节PC12细胞对NGF的反应性，从而调节Thy-1糖蛋白的表达。
