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Published on: March 8, 2015
Adenosine stimulates neuromedin U mRNA expression in the rat pars tuberalis
Sayaka Aizawa1, Tingting Gu1, Arisa Kaminoda1
1Department of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, 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.
Insights
Adenosine stimulates Neuromedin U (NMU) expression in the rat pars tuberalis (PT) via the adenosine receptor A2b and cAMP pathway. This reveals adenosine as a central metabolic signal regulating NMU, alongside melatonin.
Area of Science:
- Neuroendocrinology
- Molecular signaling
Background:
- Neuromedin U (NMU) exhibits circadian expression in the rat pars tuberalis (PT).
- Melatonin is known to suppress NMU expression in the PT.
Purpose of the Study:
- To investigate the role of adenosine in regulating Nmu expression in the rat PT.
- To elucidate the signaling pathway involved in adenosine-mediated Nmu regulation.
Main Methods:
- Assessment of adenosine receptor A2b expression in the rat PT.
- Stimulation of Nmu expression using an adenosine receptor agonist (NECA) in brain slice cultures.
- In vitro promoter assays to determine the mechanism of NECA action.
- Measurement of phosphorylated CRE-binding protein levels.
Main Results:
- The rat PT expresses adenosine receptor A2b.
- NECA significantly stimulated Nmu expression in rat brain slice cultures.
- NECA enhanced Nmu promoter activity via a cAMP response element (CRE) dependent on adenosine receptor A2b.
- NECA increased phosphorylated CRE-binding protein levels.
Conclusions:
- Adenosine stimulates Nmu expression in the rat PT through the adenosine receptor A2b and the cAMP signaling pathway.
- This study identifies adenosine as a novel regulator of Nmu expression in the PT, acting as an internal metabolic signal.
- Adenosine's role complements melatonin's function as an external environmental signal in regulating NMU in the PT.
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