1. Adenosine stimulates neuromedin U mRNA expression in the rat pars tuberalis
- Author
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Sayaka Aizawa, Ichiro Sakata, Ryuya Fujioka, Arisa Kaminoda, Sumio Takahashi, Sakae Takeuchi, Takafumi Sakai, Maho Ogoshi, Tingting Gu, and Fumiya Ojima
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,Adenosine ,Response element ,030209 endocrinology & metabolism ,Receptor, Adenosine A2B ,Biochemistry ,Second Messenger Systems ,Melatonin ,03 medical and health sciences ,0302 clinical medicine ,Endocrinology ,Slice preparation ,Internal medicine ,medicine ,Cyclic AMP ,Animals ,RNA, Messenger ,Molecular Biology ,Chemistry ,Neuropeptides ,Adenosine receptor ,Adenosine Receptor A2b ,Rats, Inbred F344 ,Rats ,030104 developmental biology ,Gene Expression Regulation ,Pituitary Gland ,Pars tuberalis ,Neuromedin U ,medicine.drug - Abstract
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.
- Published
- 2019