神经生长因子介导的克隆性嗜铬细胞瘤细胞系中酪氨酸羟化酶的诱导
Nerve growth factor-mediated induction of tyrosine hydroxylase in a clonal pheochromocytoma cell line.
作者信息
Goodman R, Herschman H R
出版信息
Proc Natl Acad Sci U S A. 1978 Sep;75(9):4587-90. doi: 10.1073/pnas.75.9.4587.
Abstract
We have established a clonal cell line, PC-G2, from an experimentally induced rat pheochromocytoma. Administration of nerve growth factor to PC-G2 causes a 4- to 8-fold induction in the specific activity of tyrosine hydroxylase [tyrosine 3-monooxygenase; L-tyrosine,tetrahydropteridine:oxygen oxidoreductase(3-hydroxylating); EC 1.14.16.2]. The response is elicited in a dose-dependent fashion, at concentrations above 0.1 microgram/ml. Antiserum to nerve growth factor inhibited the induction of tyrosine hydroxylase. Dexamethasone enhances the nerve growth factor-mediated elevation of tyrosine hydroxylase. After 3--4 days of exposure to nerve growth factor the maximal induction of tyrosine hydroxylase is seen, although a significant increase can be observed after 24 hr. In contrast to the PC-12 cell line (derived from the same tumor), in which neurite outgrowth occurs in response to nerve growth factor, there is no morphological change or alteration in growth rate of PC-G2 cells after exposure to nerve growth factor.
摘要
我们从实验诱导的大鼠嗜铬细胞瘤中建立了一个克隆细胞系PC-G2。向PC-G2细胞系施用神经生长因子会导致酪氨酸羟化酶[酪氨酸3-单加氧酶；L-酪氨酸，四氢蝶呤：氧氧化还原酶(3-羟化)；EC 1.14.16.2]的比活性提高4至8倍。在浓度高于0.1微克/毫升时，以剂量依赖方式引发该反应。抗神经生长因子血清抑制酪氨酸羟化酶的诱导。地塞米松增强神经生长因子介导的酪氨酸羟化酶升高。在暴露于神经生长因子3至4天后，可观察到酪氨酸羟化酶的最大诱导，尽管在24小时后即可观察到显著增加。与PC-12细胞系（源自同一肿瘤）不同，PC-12细胞系在暴露于神经生长因子时会发生神经突生长，而PC-G2细胞在暴露于神经生长因子后没有形态变化或生长速率改变。
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