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Increase of Calmodulin III Gene Expression by μ-Opioid Receptor Stimulation in PC12 Cells

机译:μ阿片受体刺激PC12细胞中钙调蛋白III基因表达的增加。

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References(38) Cited-By(6) Calmodulin (CaM) is a principal multifunctional mediator of Ca2+ signaling in cells. It is reported that morphine increases CaM contents in mouse brain. However, the precise mechanism of CaM induction by morphine is unknown. We investigated the changes of CaM by opioid receptor stimulation in mRNA and protein levels. Expression of CaM was increased in dose- and time-dependent manners by morphine with RT-PCR assay in PC12 cells, and naloxone inhibited the effect of morphine. The expression was also increased with DAMGO (μ-opioid agonist), but not by DPDPE (δ) and U50488 (κ). Northern blot analysis revealed that the CaMIII gene was responsive to morphine or DAMGO. CaM protein increased by DAMGO were distributed in both soluble and membranous fractions in the cells. Taken together, the data suggest that morphine induces the expression of CaMIII gene through μ-opioid receptor stimulation.
机译:参考文献(38)Cited-By(6)Calmodulin(CaM)是细胞中Ca2 +信号传导的主要多功能介体。据报道吗啡会增加小鼠大脑中CaM的含量。但是,吗啡诱导CaM的确切机制尚不清楚。我们调查了阿片受体刺激mRNA和蛋白水平中CaM的变化。 RT-PCR法检测吗啡在PC12细胞中CaM的表达呈剂量和时间依赖性,纳洛酮抑制吗啡的作用。 DAMGO(μ阿片类激动剂)的表达也增加了,但DPDPE(δ)和U50488(κ)没有增加。 Northern印迹分析表明,CaMIII基因对吗啡或DAMGO有反应。 DAMGO增加的CaM蛋白分布在细胞的可溶性和膜级组分中。两者合计,数据表明吗啡通过μ阿片受体的刺激诱导CaMIII基因的表达。

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