TY - JOUR
T1 - IgE-induced degranulation of mucosal mast cells is negatively regulated via nicotinic acetylcholine receptors
AU - Kageyama-Yahara, Natsuko
AU - Suehiro, Yoko
AU - Yamamoto, Takeshi
AU - Kadowaki, Makoto
N1 - Funding Information:
We thank Dr. Tatsuo Katagiri, Dr. Hiroshi Tsuneki and Mr. Noboru Tani (University of Toyama) and Dr. Hironori Higashio (University of Tokushima) for their technical advice. This research was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (No. 18590507) and by a grant from the Smoking Research Foundation to M. Kadowaki.
PY - 2008/12/5
Y1 - 2008/12/5
N2 - The autonomic nervous system is known to mediate mast cell activation. We investigated expression of nicotinic acetylcholine receptors (nAChRs) in mucosal-type mast cells and their contribution to the regulation of mast cell activation. Expression of mRNA of nAChR α4, α7, and β2 subunits were detected in specially differentiated mucosal-type murine bone marrow-derived mast cells (mBMMCs). Pretreatment with non-specific nAChRs agonists, acetylcholine, nicotine and epibatidine and a specific α7 subunit agonist GTS-21 significantly inhibited antigen-induced degranulation of mBMMCs in a dose-dependent manner and GTS-21-induced inhibition was significantly blocked by α7 subunit antagonist, α-bungarotoxin. Furthermore, confocal microscopy also demonstrated surface binding of α-bungarotoxin on mBMMCs. Our findings indicate that mucosal mast cell activation may be negatively regulated mainly through nAChR α7 subunit, suggesting that nAChRs are involved in neuronal-mucosal mast cell interactions.
AB - The autonomic nervous system is known to mediate mast cell activation. We investigated expression of nicotinic acetylcholine receptors (nAChRs) in mucosal-type mast cells and their contribution to the regulation of mast cell activation. Expression of mRNA of nAChR α4, α7, and β2 subunits were detected in specially differentiated mucosal-type murine bone marrow-derived mast cells (mBMMCs). Pretreatment with non-specific nAChRs agonists, acetylcholine, nicotine and epibatidine and a specific α7 subunit agonist GTS-21 significantly inhibited antigen-induced degranulation of mBMMCs in a dose-dependent manner and GTS-21-induced inhibition was significantly blocked by α7 subunit antagonist, α-bungarotoxin. Furthermore, confocal microscopy also demonstrated surface binding of α-bungarotoxin on mBMMCs. Our findings indicate that mucosal mast cell activation may be negatively regulated mainly through nAChR α7 subunit, suggesting that nAChRs are involved in neuronal-mucosal mast cell interactions.
KW - Bone marrow-derived mast cells
KW - Degranulation
KW - Mucosal mast cells
KW - Nicotinic acetylcholine receptors
UR - http://www.scopus.com/inward/record.url?scp=54449092946&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2008.10.004
DO - 10.1016/j.bbrc.2008.10.004
M3 - 学術論文
C2 - 18848921
AN - SCOPUS:54449092946
SN - 0006-291X
VL - 377
SP - 321
EP - 325
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -