Fluoxetine increases the expression of NCAM140 and pCREB in rat C6 glioma cells.
Fluoxetine increases the expression of NCAM140 and pCREB in rat C6 glioma cells.
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DOI：
10.4306/pi.2012.9.2.180
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发表时间：
2012-06
影响因子：
2.7
通讯作者：
Chai YG
中科院分区：
文献类型：
--
作者：
Choi MR;Oh DH;Kim SH;Jung KH;Das ND;Chai YG
众所周知，大脑中神经可塑性的功能障碍会改变神经网络，从而导致抑郁症。为了了解氟西汀如何调节神经可塑性相关分子，我们检测了氟西汀治疗后大鼠C6胶质瘤细胞中NCAM、NCAM140、CREB和pCREB的表达水平。10µM氟西汀作用20 min、6、24、72 h后培养C6细胞。免疫细胞化学检测氟西汀对NCAM表达的影响。Western blot检测氟西汀治疗后NCAM140和CREB的表达水平以及pCREB的诱导情况。与对照细胞相比，氟西汀处理72 h后细胞膜周围NCAM表达显著增加。氟西汀处理6和72 h的细胞与处理20 min的细胞相比，NCAM140的表达显著增加。氟西汀处理72 h后，细胞中pCREB水平不仅升高60%以上，而且与其他处理时间相比也有显著差异。氟西汀处理72 h后，C6细胞NCAM140水平升高，CREB磷酸化水平升高。我们的研究结果表明，氟西汀治疗通过NCAM140同源相互作用诱导Ras-MAPK通路的激活，磷酸化并激活CREB，从而调节神经元可塑性和神经突生长。
Dysfunction of neural plasticity in the brain is known to alter neural networks, resulting in depression. To understand how fluoxetine regulates molecules involved in neural plasticity, the expression levels of NCAM, NCAM140, CREB and pCREB, in rat C6 glioma cells after fluoxetine treatment were examined. C6 cells were cultured after 20 min or after 6, 24 or 72 h treatments with 10 µM fluoxetine. Immunocytochemistry was used to determine the effect of fluoxetine on the expression of NCAM. Western blot analysis was used to measure the expression levels of NCAM140 and CREB and the induction of pCREB after fluoxetine treatment. NCAM expression following 72-h fluoxetine treatment was significantly increased around cell membranes compared to control cells. Cells treated with fluoxetine for 6 and 72 h showed a significant increase in NCAM140 expression compared to cells treated for 20 min. The level of pCREB in the cells treated with fluoxetine for 72 h not only increased more than 60%, but was also significantly different when compared with the other treatment times. The 72-h fluoxetine treatment led to the increase of NCAM140 and the phosphorylation of CREB in C6 cells. Our findings indicate that fluoxetine treatment regulates neuronal plasticity and neurite outgrowth by phosphorylating and activating CREB via the NCAM140 homophilic interaction-induced activation of the Ras-MAPK pathway.
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DOI：
10.1017/s1461145708009255
发表时间：
2009-04-01
影响因子：
4.8
作者：
Conboy, Lisa;Tanrikut, Cihan;Diamond, David M.
通讯作者：
Diamond, David M.
影响因子：
2.7
作者：
Choi, Mi Ran;Oh, Dong Hoon;Park, Yong-Chon
通讯作者：
Park, Yong-Chon
影响因子：
3.1
作者：
Levkovitz, Y;Gil-Ad, I;Weizman, A
通讯作者：
Weizman, A
影响因子：
--
作者：
Cotter, D;Mackay, D;Everall, I
通讯作者：
Everall, I
影响因子：
6.1
作者：
Laifenfeld, D;Karry, R;Ben-Shachar, D
通讯作者：
Ben-Shachar, D