Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells

Haruhiro Higashida; Sarah E.H. Bowden; Shigeru Yokoyama; Alla Salmina; Minako Hashii; Naoto Hoshi; Jia Sheng Zhang; Rimma Knijnik; Mami Noda; Zen Guo Zhong; Duo Jin; Kazuhiro Higashida; Hisashi Takeda; Tenpei Akita; Kenji Kuba; Sayaka Yamagishi; Noriaki Shimizu; Shin Takasawa; Hiroshi Okamoto; Jon Robbins

doi:10.1016/j.neures.2006.11.008

Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca²⁺ signalling in rodent NG108-15 neuroblastoma cells

Haruhiro Higashida, Sarah E.H. Bowden, Shigeru Yokoyama, Alla Salmina, Minako Hashii, Naoto Hoshi, Jia Sheng Zhang, Rimma Knijnik, Mami Noda, Zen Guo Zhong, Duo Jin, Kazuhiro Higashida, Hisashi Takeda, Tenpei Akita, Kenji Kuba, Sayaka Yamagishi, Noriaki Shimizu, Shin Takasawa, Hiroshi Okamoto, Jon Robbins

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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 Ca²⁺ concentrations ([Ca²⁺]_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 Ca²⁺ release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca²⁺ signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.

Original language	English
Pages (from-to)	339-346
Number of pages	8
Journal	Neuroscience Research
Volume	57
Issue number	3
DOIs	https://doi.org/10.1016/j.neures.2006.11.008
Publication status	Published - 2007 Mar

Keywords

ADP-ribosyl cyclase
CD38
Ca
Cyclic ADP-ribose
Muscarinic acetylcholine receptor

ASJC Scopus subject areas

Neuroscience(all)

Access to Document

10.1016/j.neures.2006.11.008

Cite this

Higashida, H., Bowden, S. E. H., Yokoyama, S., Salmina, A., Hashii, M., Hoshi, N., Zhang, J. S., Knijnik, R., Noda, M., Zhong, Z. G., Jin, D., Higashida, K., Takeda, H., Akita, T., Kuba, K., Yamagishi, S., Shimizu, N., Takasawa, S., Okamoto, H., & Robbins, J. (2007). Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca²⁺ signalling in rodent NG108-15 neuroblastoma cells. Neuroscience Research, 57(3), 339-346. https://doi.org/10.1016/j.neures.2006.11.008

Higashida, H, Bowden, SEH, Yokoyama, S, Salmina, A, Hashii, M, Hoshi, N, Zhang, JS, Knijnik, R, Noda, M, Zhong, ZG, Jin, D, Higashida, K, Takeda, H, Akita, T, Kuba, K, Yamagishi, S, Shimizu, N, Takasawa, S, Okamoto, H & Robbins, J 2007, 'Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca²⁺ signalling in rodent NG108-15 neuroblastoma cells', Neuroscience Research, vol. 57, no. 3, pp. 339-346. https://doi.org/10.1016/j.neures.2006.11.008

@article{106934b8857e44d795719809225b5b1b,

title = "Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells",

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 Ca2+ concentrations ([Ca2+]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 Ca2+ release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca2+ signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.",

keywords = "ADP-ribosyl cyclase, CD38, Ca, Cyclic ADP-ribose, Muscarinic acetylcholine receptor",

author = "Haruhiro Higashida and Bowden, {Sarah E.H.} and Shigeru Yokoyama and Alla Salmina and Minako Hashii and Naoto Hoshi and Zhang, {Jia Sheng} and Rimma Knijnik and Mami Noda and Zhong, {Zen Guo} and Duo Jin and Kazuhiro Higashida and Hisashi Takeda and Tenpei Akita and Kenji Kuba and Sayaka Yamagishi and Noriaki Shimizu and Shin Takasawa and Hiroshi Okamoto and Jon Robbins",

note = "Funding Information: This investigation was supported in part by a research grant (to H.H.) from the Japanese Ministry of Education, Culture, Sports, Science and Technology (to H.H.) and from the Uehara Memorial Foundation (to N.H.), and also supported by the Euro-Japan Exchange Program from the Novartis Foundation (to A.S.). We thank R. Graeff and H.-C. Lee for technical advices in cADPR measurements.",

year = "2007",

month = mar,

doi = "10.1016/j.neures.2006.11.008",

language = "English",

volume = "57",

pages = "339--346",

journal = "Neuroscience Research",

issn = "0168-0102",

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T1 - Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells

AU - Higashida, Haruhiro

AU - Bowden, Sarah E.H.

AU - Yokoyama, Shigeru

AU - Salmina, Alla

AU - Hashii, Minako

AU - Hoshi, Naoto

AU - Zhang, Jia Sheng

AU - Knijnik, Rimma

AU - Noda, Mami

AU - Zhong, Zen Guo

AU - Jin, Duo

AU - Higashida, Kazuhiro

AU - Takeda, Hisashi

AU - Akita, Tenpei

AU - Kuba, Kenji

AU - Yamagishi, Sayaka

AU - Shimizu, Noriaki

AU - Takasawa, Shin

AU - Okamoto, Hiroshi

AU - Robbins, Jon

N1 - Funding Information: This investigation was supported in part by a research grant (to H.H.) from the Japanese Ministry of Education, Culture, Sports, Science and Technology (to H.H.) and from the Uehara Memorial Foundation (to N.H.), and also supported by the Euro-Japan Exchange Program from the Novartis Foundation (to A.S.). We thank R. Graeff and H.-C. Lee for technical advices in cADPR measurements.

PY - 2007/3

Y1 - 2007/3

N2 - 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 Ca2+ concentrations ([Ca2+]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 Ca2+ release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca2+ signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.

AB - 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 Ca2+ concentrations ([Ca2+]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 Ca2+ release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca2+ signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.

KW - ADP-ribosyl cyclase

KW - CD38

KW - Ca

KW - Cyclic ADP-ribose

KW - Muscarinic acetylcholine receptor

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