Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells.
Neurosci Res
; 57(3): 339-46, 2007 Mar.
Article
em En
| MEDLINE
| ID: mdl-17173996
ABSTRACT
The role of cyclic ADP-ribose (cADPR) and its synthetic enzyme, CD38, as a downstream signal of muscarinic acetylcholine receptors (mAChRs) was examined in neuroblastoma cells expressing M1 mAChRs (NGM1). NGM1 cells were further transformed with both wild-type and mutant (C119K/C201E) human CD38. The dual transformed cells exhibited higher cADPR formation than ADPR production and elevated intracellular free Ca(2+) concentrations ([Ca(2+)](i)) in response to ACh. These phenotypes were analyzed in detail in a representative CD38 clone. The intracellular cADPR concentration by ACh application was significantly increased by CD38 overexpression. Digital image analysis by a confocal microscopy revealed that topographical distribution of the sites of Ca(2+) release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca(2+) signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.
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Base de dados:
MEDLINE
Assunto principal:
Acetilcolina
/
Receptores Muscarínicos
/
Sinalização do Cálcio
/
ADP-Ribosil Ciclase
/
ADP-Ribose Cíclica
/
ADP-Ribosil Ciclase 1
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article