Calmodulin kinase II activation of mitogen-activated protein kinase in PC12 cell following all-trans retinoic acid treatment
Calmodulin kinase II activation of mitogen-activated protein kinase in PC12 cell following all-trans retinoic acid treatment
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DOI：
10.1016/j.neuro.2009.03.006
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发表时间：
2009-07-01
期刊：
影响因子：
3.4
通讯作者：
Xie, Jun
中科院分区：
文献类型：
--
作者：
Liu, Jiangong;Zhou, Ran;Xie, Jun
先前的研究表明，细胞凋亡可以通过激活钙调蛋白激酶 II (CaMKII) 或丝裂原激活蛋白激酶 (MAPK)、ERK 和 p38 来介导。在本研究中，我们研究了 CaMKII 是否参与 PC12 细胞中全反式视黄酸 (ATRA) 处理时 ERK 和 p38 的激活。结果表明，ATRA 诱导的 ERK 和 p38 激活发生晚于 CAMKII。 siRNA 敲低 CAMKII 显着抑制 ATRA 诱导的 ERK 和 p38 激活。这些结果表明，ATRA 暴露后 ERK 和 p38 的激活是 CAMKII 依赖性的。 ATRA 治疗还导致 PC12 细胞出现以凋亡为特征的细胞死亡。结果表明，CaMKII 依赖性 ERK 和 p38 激活与细胞凋亡相关。 (C) 2009 Elsevier Inc. 保留所有权利。
Previous studies have shown that apoptosis can be mediated by activation of either calmodulin kinase II (CaMKII) or mitogen-activated protein kinase (MAPK), ERK and p38. In the present study, we investigated whether CaMKII is involved in activation of ERK and p38 in response to all-trans retinoic acid (ATRA) treatment in PC12 cells. Results showed that ATRA-induced activation of ERK and p38 occurred later than that of CAMKII. Knockdown of CAMKII by siRNA significantly suppressed ATRA-induced activation of ERK and p38. These results demonstrated that activation of ERK and p38 following ATRA exposure is CAMKII-dependent. Treatment with ATRA also resulted in cell death characterized by apoptosis in PC12 cells. Results suggest that CaMKII-dependent activation of ERK and p38 is related to apoptotic cell death. (C) 2009 Elsevier Inc. All rights reserved.