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Mol Cell Endocrinol. 2019 Oct 1;496:110518. doi: 10.1016/j.mce.2019.110518. Epub 2019 Jul 22.

Adenosine stimulates neuromedin U mRNA expression in the rat pars tuberalis.

Author information

1
Department of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan. Electronic address: saizawa@okayama-u.ac.jp.
2
Department of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
3
Department of Natural Sciences and Biology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan.
4
Area of Regulatory Biology, Division of Life Science, Graduate School of Science and Engineering, Saitama University, 255 Shimo-ohkubo, Sakuraku, Saitama, 338-8570, Japan.

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.

KEYWORDS:

Adenosine receptor; Circadian rhythm; Melatonin; Neuromedin U; Pars tuberalis; cAMP response element

PMID:
31344393
DOI:
10.1016/j.mce.2019.110518

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