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eCAM Advance Access published online on October 29, 2007
eCAM, doi:10.1093/ecam/nem146
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© 2007 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

AMP N1-oxide, a unique compound of royal jelly, induces neurite outgrowth from PC12 cells via signaling by protein kinase A independent of that by mitogen-activated protein kinase

Noriko Hattori1,2, Hiroshi Nomoto1, Hidefumi Fukumitsu1, Satoshi Mishima2 and Shoei Furukawa1

1Laboratory of Molecular Biology, Gifu Pharmaceutical University, Mitahora-higashi, Gifu 502-8585, Japan and 2Nagaragawa Research Center, API Co., Ltd, Nagara, Gifu 502-0071, Japan

Earlier we identified adenosine monophosphate (AMP) N1-oxide as a unique compound of royal jelly (RJ) that induces neurite outgrowth (neuritegenesis) from cultured rat pheochromocytoma PC12 cells via the adenosine A2A receptor. Now, we found that AMP N1-oxide stimulated the phosphorylation of not only mitogen-activated protein kinase (MAPK) but also that of cAMP/calcium-response element-binding protein (CREB) in a dose-dependent manner. Inhibition of MAPK activation by a MEK inhibitor, PD98059, did not influence the AMP N1-oxide-induced neuritegenesis, whereas that of protein kinase A (PKA) by a selective inhibitor, KT5720, significantly reduced neurite outgrowth. AMP N1-oxide also had the activity of suppressing the growth of PC12 cells, which correlated well with the neurite outgrowth-promoting activity. KT5720 restored the growth of AMP N1-oxide-treated PC12 cells. It is well known that nerve growth factor suppresses proliferation of PC12 cells before causing stimulation of neuronal differentiation. Thus, AMP N1-oxide elicited neuronal differentiation of PC12 cells, as evidenced by generation of neurites, and inhibited cell growth through adenosine A2A receptor-mediated PKA signaling, which may be responsible for characteristic actions of RJ.

Keywords: adenosine A2A receptor – 5-bromodeoxy uridine – neuronal differentiation – neurotrophic factor

For all reprints and correspondence: Shoei Furukawa, Laboratory of Molecular Biology, Gifu Pharmaceutical University, 5-6-1, Mitahora-higashi, Gifu 502-8585, Japan. Tel/Fax: +81-58-237-8589; E-mail: furukawa{at}gifu-pu.ac.jp

Received May 12, 2007; accepted August 20, 2007


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