TY - JOUR
T1 - Inositol trisphosphate/Ca2+ as messengers of bradykinin B2 and muscarinic acetylcholine m1-m4 receptors in neuroblastoma-derived hybrid cells
AU - Noda, Mami
AU - Ishizaka, Nobuto
AU - Yokoyama, Shigeru
AU - Hoshi, Naoto
AU - Kimura, Yasuhiro
AU - Hashii, Minako
AU - Taketo, Megumi
AU - Egorova, Alla
AU - Knijnik, Rimma
AU - Fukuda, Kazuhiko
AU - Morikawa, Hitoshi
AU - Brown, David A.
AU - Higashida, Haruhiro
PY - 1996/9
Y1 - 1996/9
N2 - Neuroblastoma x glioma hybrid NG108-15 and neuroblastoma x fibroblast hybrid NL308 cells possess endogenous bradykinin B2 receptors and m4 muscarinic acetylcholine receptors (mAChRs), which couple to phospholipase C and adenylate cyclase, respectively. Four genetic subtypes of mAChRs differed in their effects when stimulated in NG108-15 and NL308 cells overexpressing mAChRs. Broadly speaking, the principal effects fell into two categories: the odd-numbered receptors (m1 and m3) activated phospholipase C and increased inositol trisphosphate/Ca2+, as bradykinin did, whereas the even-numbered receptors (m2 and m4) inhibited adenylate cyclase via a pertussis toxin (PTx)-sensitive G-protein in NG108-15 cells. But all four types of NL308 cells overexpressing each m1, m2, m3 and m4 receptor activated phospholipase C, while keeping the PTx-sensitivity in m2/m4, but not in m1/m3 receptors. Coupling to ion channel effectors showed a comparable dichotomy in NG108-15 cells, while cross-activation occurred in NL308 cells.
AB - Neuroblastoma x glioma hybrid NG108-15 and neuroblastoma x fibroblast hybrid NL308 cells possess endogenous bradykinin B2 receptors and m4 muscarinic acetylcholine receptors (mAChRs), which couple to phospholipase C and adenylate cyclase, respectively. Four genetic subtypes of mAChRs differed in their effects when stimulated in NG108-15 and NL308 cells overexpressing mAChRs. Broadly speaking, the principal effects fell into two categories: the odd-numbered receptors (m1 and m3) activated phospholipase C and increased inositol trisphosphate/Ca2+, as bradykinin did, whereas the even-numbered receptors (m2 and m4) inhibited adenylate cyclase via a pertussis toxin (PTx)-sensitive G-protein in NG108-15 cells. But all four types of NL308 cells overexpressing each m1, m2, m3 and m4 receptor activated phospholipase C, while keeping the PTx-sensitivity in m2/m4, but not in m1/m3 receptors. Coupling to ion channel effectors showed a comparable dichotomy in NG108-15 cells, while cross-activation occurred in NL308 cells.
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U2 - 10.1016/0929-7855(96)00523-8
DO - 10.1016/0929-7855(96)00523-8
M3 - Article
C2 - 8906560
AN - SCOPUS:0030222499
SN - 1098-8823
VL - 14
SP - 175
EP - 185
JO - Journal of Lipid Mediators
JF - Journal of Lipid Mediators
IS - 1-3
ER -