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首页> 外文期刊>Signal transduction: Receptors, mediators and genes: Official journal of the Signal Transduction Society >Serotonin 1A receptor coupling to NF-B studied using inducible receptor expression in hippocampal neuron-derived cells
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Serotonin 1A receptor coupling to NF-B studied using inducible receptor expression in hippocampal neuron-derived cells

机译：使用海马神经元衍生细胞中诱导型受体表达研究血清素1A受体与NF-B的耦合

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The mechanism of serotonin 1A receptor (5-HT1A-R) mediated activation of NF-B has been studied in non-neural cells, but this pathway has not been elucidated in neuronal cells. We have used inducible expression of the 5-HT1A-R in the hippocampal neuron-derived HN2 cells to analyze the coupling of this receptor to NF-B. A construct harboring luciferase cDNA driven by a minimal promoter under the control of an NF-B-specific enhancer element was transfected into these 5-HT1A-R-expressing HN2 cells. Using luciferase expression in the transfected cells, we have studied 5-HT1A-R agonist evoked activation of NF-B. Inhibition of either mitogen activated protein kinase (MAPK) pathway with PD98059 or protein kinase C (PKC) with GFX caused elevation of the basal level of NF-B activity but did not affect 5-HT1A-R mediated activation of NF-B. Furthermore, neither the basal level of NF-B nor its activation by a 5-HT1A-R agonist was altered by dibutyrylcAMP. Thus, the MAPK pathway and PKC cause inhibition of the basal NF-B activity and the 5-HT1A-R-linked NF-B activation does not require MAPK, PKC, and cAMP. Intriguingly, Western blot analysis showed that 5-HT1A-R mediates activation of both CaMKII and PI-3K. This 5-HT1A-R-evoked the stimulation of CaMKII was reversed in the presence of a PI-3K inhibitor. Therefore, the likely mechanism of 5-HT1A-R mediated induction of NF-B in neuronal cells involves activation of PI-3K upstream of CaMKII. This reveals a novel pathway that could be crucial in the functional activity of brain neurons.
机译：已在非神经细胞中研究了血清素1A受体（5-HT1A-R）介导的NF-B激活机制，但在神经元细胞中尚未阐明该途径。我们已经使用了海马神经元来源的HN2细胞中5-HT1A-R的可诱导表达来分析该受体与NF-B的偶联。将含有由最小启动子驱动的荧光素酶cDNA的构建体在NF-B特异性增强子的控制下转染到这些表达5-HT1A-R的HN2细胞中。使用荧光素酶在转染细胞中的表达，我们研究了5-HT1A-R激动剂引起的NF-B激活。用PD98059抑制有丝分裂原活化的蛋白激酶（MAPK）途径或用GFX抑制蛋白激酶C（PKC）引起基础水平的NF-B活性升高，但不影响5-HT1A-R介导的NF-B活化。此外，双丁酰氨并没有改变NF-B的基础水平或5-HT1A-R激动剂对其的激活。因此，MAPK途径和PKC导致对基础NF-B活性的抑制，并且5-HT1A-R连接的NF-B激活不需要MAPK，PKC和cAMP。有趣的是，蛋白质印迹分析表明5-HT1A-R介导了CaMKII和PI-3K的激活。在PI-3K抑制剂存在下，这种5-HT1A-R引起的CaMKII刺激被逆转。因此，神经元细胞中5-HT1A-R介导的NF-B诱导的可能机制涉及CaMKII上游PI-3K的激活。这揭示了一条可能对脑神经元功能活动至关重要的新途径。

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