[1]李宏维,周斌,张海鸿.TRPM8通过cAMP-PKA/UCP4信号调控氧糖剥夺/复糖复氧诱导的神经元凋亡[J].南方医科大学学报,2016,(09):1265.
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TRPM8通过cAMP-PKA/UCP4信号调控氧糖剥夺/复糖复氧诱导的神经元凋亡()
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《南方医科大学学报》[ISSN:/CN:]

卷:
期数:
2016年09期
页码:
1265
栏目:
出版日期:
2016-09-16

文章信息/Info

Title:
TRPM8 mediates PC-12 neuronal cell apoptosis induced by oxygen-glucose deprivation through cAMP-PKA/UCP4 signaling
作者:
李宏维周斌张海鸿
关键词:
PC12细胞氧糖剥夺/复糖复氧TRPM8cAMP-PKA/UCP4凋亡
Keywords:
PC12 cells oxygen-glucose deprivation TRPM8 cAMP-PKA/UCP4 apoptosis
摘要:
目的探究TRPM8在氧糖剥夺/复糖复氧诱导神经元PC12细胞凋亡中的分子机制。方法体外建立氧糖剥夺/复糖复氧模 型模拟脊髓缺血再灌注损伤,流式细胞仪检测PC12细胞的凋亡,RT-PCR和western blot检测TRPM8、UCP4和cAMP、p-PKA、 Bax、Bcl-2 的表达变化;向PC12 细胞分别加入AMTB(TRPM8 阻断剂)和转染UCP4 质粒,western blot 检测cAMP、p-PKA、 UCP4、Bax、Bcl-2的表达水平;抑制PKA信号,检测UCP4、Bax、Bcl-2的蛋白表达水平。结果氧糖剥夺/复糖复氧导致脊髓神经 元PC12 细胞发生凋亡,TRPM8 过表达,UCP4 表达下降,抑制cAMP-PKA 信号。抑制TRPM8 表达,则细胞凋亡减少, cAMP-PKA信号被激活,且UCP4的表达有所恢复。抑制TRPM8和cAMP-PKA信号,UCP4的表达减少,细胞凋亡增加。结论 在氧糖剥夺/复糖复氧模型中,PC12细胞TRPM8过表达,且通过cAMP-PKA/UCP4诱导神经元PC12细胞凋亡。
Abstract:
Objective To explore the molecular mechanism responsible for apoptosis of PC-12 neuronal cells induced by oxygen-glucose deprivation (OGD). Methods PC12 cells were exposed to OGD for 24 h to simulate ischemia-reperfusion injury. Flow cytometry was employed detect the cell apoptosis, and the expresions of TRPM8, UCP4, cAMP and PKA in the exposed cells were detected with RT-PCR and Western blotting. The changes in the expressions of Bax, Bcl-2, cAMP, PKA and UCP4 proteins were detected in the exposed cells in resposne to inhibition of TRPM8 and cAMP-PKA signal or over-expression of UCP4. Results OGD for 24 induced obvious apoptosis in PC-12 cells and caused TRPM8 over-expression and inhibition of UCP4 and cAMP-PKA signaling. Inhibiting TRPM8 expression reduced the cell apoptosis and up-regulated cAMP, p-PKA and UCP4 in the cells exposed to OGD. In cells exposed to OGD, inhibition of TRPM8 and cAMP-PKA signaling suppressed the expressio of UCP4 and increased the cell apoptosis. Conclusion TRPM8 mediates OGD-induced PC12 cell apoptosis through cAMP-PKA/UCP4 signaling.

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更新日期/Last Update: 1900-01-01