Differential role of ERK in cAMP-induced Nurr1 expression in N2A and C6 cells.
Differential role of ERK in cAMP-induced Nurr1 expression in N2A and C6 cells.
复制标题
ERK 在 N2A 和 C6 细胞中 cAMP 诱导的 Nurr1 表达中的不同作用。
DOI：
10.1097/00001756-200401190-00020
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发表时间：
2004
期刊：
影响因子：
1.7
通讯作者：
Nikodem,VeraM
中科院分区：
文献类型：
--
作者：
Lee,MiKyeong;Nikodem,VeraM
我们研究了在神经母细胞瘤N2A和C6胶质瘤细胞系中与cAMP诱导转录因子Nurr 1相关的信号通路。Nurr1的表达诱导forskolin，腺苷酸环化酶激活剂，通过激活CREB在N2A和C6细胞。然而，毛喉素对ERK的作用是细胞特异性的。在N2A细胞中，毛喉素刺激ERK磷酸化，而在C6细胞中则抑制ERK磷酸化。PKA抑制剂H89预处理可阻断Forskolin诱导的Nurr1在N2A和C6细胞中的表达。有趣的是，用MEK抑制剂PD98059预处理显示出不同的效果。用PD98059预处理抑制N2A细胞中Forskolin诱导的Nurr1表达，然而，在C6细胞中，Nurr1表达进一步增加。我们的研究结果表明，ERK通路在cAMP诱导的N2A和C6细胞Nurr1表达中起着不同的作用。
We investigated the signal pathway related to induction of Nurr1, transcription factor, by cAMP in neuroblastoma N2A and C6 glioma cell lines. Nurr1 expression was induced by forskolin, an adenylate cyclase activator, via activation of CREB in both N2A and C6 cells. The effect of forskolin on ERK, however, was cell specific. ERK phosphorylation was stimulated by forskolin in N2A cells whereas it was inhibited in C6 cells. Pretreatment with H89, a PKA inhibitor, blocked the forskolin-induced Nurr1 expression in both N2A and C6 cells. Interestingly, pretreatment with PD98059, an MEK inhibitor, showed differential effects. Pretreatment with PD98059 inhibited the forskolin-induced Nurr1 expression in N2A cells, however, in C6 cells, Nurr1 expression was further increased. Our results suggest that ERK pathway plays a differential role in cAMP-induced Nurr1 expression in N2A and C6 cells.