2011 Fiscal Year Final Research Report
Involvement of a non-neuronal cardiac cholinergic system in energy metabolism and pathophysiological situations
| Project/Area Number |
21590283
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Kochi University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SATO Takayuki 高知大学, 教育研究部・医療学系, 教授 (90205930)
ARIKAWA Mikihiko 高知大学, 教育研究部・医療学系, 助教 (20432817)
NOGUCHI Tatsuya 高知大学, 教育研究部・医療学系, 助教 (50566495)
ZHENG Can 高知大学, 教育研究部・医療学系, 助教 (50443495)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 心血管 / 血液 / アセチルコリン |
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| Research Abstract |
We have so far reported novel effects of parasympathetic nerve system-derived ACh in the cardiovascular system. Recently it has been reported that a cholinergic system is composed of a classical parasympathetic nerve system and a non-neuronal cholinergic system. The classical parasympathetic nerve system plays a role in inhibiting a function of sympathetic nerve system, i. e., decreasing of heart rate and cardiac contraction. In contrast, the non-neuronal cholinergic system means that ACh is synthesized by a cell at its local site, and a non-neuronal cardiac cholinergic system is that one cardiomyocytes synthesizes ACh independently from the classical parasympathetic nerve system. Novel functions of ACh other than modulating sympathetic nerve, which we have identified, includes anti-arrhythmogenic effects, anti-apoptotic effects, hypoxia tolerance effects and angiogenesis accelerating effects. It is expected that those effects are also regulated by the non-neuronal cardiac cholinergic system. In the current study, we have revealed that this system plays a role in negatively regulating cellular energy metabolism, preventing cells from overshooting oxygen consumption leading to cell protection, and that this system is upregulated by pharmacological intervention and some manipulation other than drugs. Taken together, these results raise a possibility that this system can be a therapeutic target and a tool to profoundly understand a pathophysiology of cardiovascular diseases.
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[Presentation] Molecular mechanisms of muscular abnormality in transgenic mice overexpressing NF90, a dsRNA binding protein2011
Author(s)
Sakamoto S, Higuchi T, Kakinuma Y, Kai S, Todaka H, Yagyu K, Obata E, Morisawa K, Fukushima A, Tsuda M, Taniguchi T
Organizer
16^<th> Annual Meeting of the RNA Society
Place of Presentation
Kyoto, Japan
Year and Date
20110614-18
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