Adenosine stimulates neuromedin U mRNA expression in the rat pars tuberalis
Adenosine stimulates neuromedin U mRNA expression in the rat pars tuberalis
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DOI：
10.1016/j.mce.2019.110518
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发表时间：
2019-10-01
影响因子：
4.1
通讯作者：
Takeuchi, Sakae
中科院分区：
文献类型：
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作者：
Aizawa, Sayaka;Gu, Tingting;Takeuchi, Sakae
神经medin U （NMU）在大鼠结节部（PT）中显示昼夜节律表达，并被褪黑激素抑制。在这里，我们研究了腺苷参与调节Nmu的表达。我们发现大鼠PT表达腺苷受体A2b，腺苷受体激动剂NECA刺激脑切片培养中Nmu的表达。体外启动子实验表明，在腺苷受体A2b存在的情况下，NECA通过cAMP反应元件（CRE）刺激Nmu启动子活性。NECA还增加了磷酸化cre结合蛋白的水平。这些研究结果表明，腺苷通过腺苷受体A2b激活大鼠PT中cAMP信号通路，从而刺激Nmu的表达。这是第一个证明PT中Nmu的表达受腺苷的调节，除了褪黑素作为外部光周期环境信号外，腺苷还作为一种生命中枢代谢信号。
Neuromedin U (NMU) shows circadian expression in the rat pars tuberalis (PT), and is known to be suppressed by melatonin. Here we examined the involvement of adenosine in the regulation of Nmu expression. We found that the rat PT expressed adenosine receptor A2b and that an adenosine receptor agonist, NECA, stimulated Nmu expression in brain slice cultures. In vitro promoter assays revealed that NECA stimulated Nmu promoter activity via a cAMP response element (CRE) in the presence of adenosine receptor A2b. NECA also increased the levels of phosphorylated CRE-binding protein. These findings suggest that adenosine stimulates Nmu expression by activating the cAMP signaling pathway through adenosine receptor A2b in the rat PT. This is the first report to demonstrate that Nmu expression in the PT is regulated by adenosine, which acts as an intravital central metabolic signal, in addition to melatonin, which acts as an external photoperiodic environmental signal.