Signaling involved in pituitary adenylate cyclase-activating polypeptide-stimulated ADNP expression

Tomoya Nakamachi; Min Li; Seiji Shioda; Akira Arimura

doi:10.1016/j.peptides.2006.01.007

Signaling involved in pituitary adenylate cyclase-activating polypeptide-stimulated ADNP expression

Tomoya Nakamachi, Min Li, Seiji Shioda, Akira Arimura^*

^*Corresponding author for this work

Department of Biology

Research output: Contribution to journal › Article › peer-review

37 Scopus citations

Abstract

Activity-dependent neurotrophic protein (ADNP) was discovered as a novel response gene for VIP and has neuroprotective potential. When the VIP paralog, PACAP38 was added to mouse neuron-glia co-cultures, it induced ADNP mRNA expression in a bimodal fashion at subpico- and nanomolar concentrations with greater response at subpicomolar level. The response was attenuated by a PAC1-R antagonist at both concentrations and by a VPAC1-R antagonist at nanomolar concentration only. An IP3/PLC inhibitor attenuated the response at both concentrations of PACAP38, but a MAPK inhibitor had no effect. A PKA inhibitor suppressed the response at nanomolar concentration only. These findings suggest that ADNP expression is mediated through multiple receptors and signaling pathways that are regulated by different concentrations of PACAP.

Original language	English
Pages (from-to)	1859-1864
Number of pages	6
Journal	Peptides
Volume	27
Issue number	7
DOIs	https://doi.org/10.1016/j.peptides.2006.01.007
State	Published - 2006/07

Keywords

ADNP
Mouse
Neuron/glia co-culture
PACAP
Signal transduction

ASJC Scopus subject areas

Biochemistry
Physiology
Endocrinology
Cellular and Molecular Neuroscience

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10.1016/j.peptides.2006.01.007

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title = "Signaling involved in pituitary adenylate cyclase-activating polypeptide-stimulated ADNP expression",

abstract = "Activity-dependent neurotrophic protein (ADNP) was discovered as a novel response gene for VIP and has neuroprotective potential. When the VIP paralog, PACAP38 was added to mouse neuron-glia co-cultures, it induced ADNP mRNA expression in a bimodal fashion at subpico- and nanomolar concentrations with greater response at subpicomolar level. The response was attenuated by a PAC1-R antagonist at both concentrations and by a VPAC1-R antagonist at nanomolar concentration only. An IP3/PLC inhibitor attenuated the response at both concentrations of PACAP38, but a MAPK inhibitor had no effect. A PKA inhibitor suppressed the response at nanomolar concentration only. These findings suggest that ADNP expression is mediated through multiple receptors and signaling pathways that are regulated by different concentrations of PACAP.",

keywords = "ADNP, Mouse, Neuron/glia co-culture, PACAP, Signal transduction",

author = "Tomoya Nakamachi and Min Li and Seiji Shioda and Akira Arimura",

note = "Funding Information: The authors thank Drs. Harold Dundee and Hirokazu Ohtaki for their editorial assistance on this manuscript. This work was supported in part by the Kaken American Foundation.",

year = "2006",

month = jul,

doi = "10.1016/j.peptides.2006.01.007",

language = "英語",

volume = "27",

pages = "1859--1864",

journal = "Peptides",

issn = "0196-9781",

publisher = "Elsevier Inc.",

number = "7",

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TY - JOUR

T1 - Signaling involved in pituitary adenylate cyclase-activating polypeptide-stimulated ADNP expression

AU - Nakamachi, Tomoya

AU - Li, Min

AU - Shioda, Seiji

AU - Arimura, Akira

N1 - Funding Information: The authors thank Drs. Harold Dundee and Hirokazu Ohtaki for their editorial assistance on this manuscript. This work was supported in part by the Kaken American Foundation.

PY - 2006/7

Y1 - 2006/7

N2 - Activity-dependent neurotrophic protein (ADNP) was discovered as a novel response gene for VIP and has neuroprotective potential. When the VIP paralog, PACAP38 was added to mouse neuron-glia co-cultures, it induced ADNP mRNA expression in a bimodal fashion at subpico- and nanomolar concentrations with greater response at subpicomolar level. The response was attenuated by a PAC1-R antagonist at both concentrations and by a VPAC1-R antagonist at nanomolar concentration only. An IP3/PLC inhibitor attenuated the response at both concentrations of PACAP38, but a MAPK inhibitor had no effect. A PKA inhibitor suppressed the response at nanomolar concentration only. These findings suggest that ADNP expression is mediated through multiple receptors and signaling pathways that are regulated by different concentrations of PACAP.

AB - Activity-dependent neurotrophic protein (ADNP) was discovered as a novel response gene for VIP and has neuroprotective potential. When the VIP paralog, PACAP38 was added to mouse neuron-glia co-cultures, it induced ADNP mRNA expression in a bimodal fashion at subpico- and nanomolar concentrations with greater response at subpicomolar level. The response was attenuated by a PAC1-R antagonist at both concentrations and by a VPAC1-R antagonist at nanomolar concentration only. An IP3/PLC inhibitor attenuated the response at both concentrations of PACAP38, but a MAPK inhibitor had no effect. A PKA inhibitor suppressed the response at nanomolar concentration only. These findings suggest that ADNP expression is mediated through multiple receptors and signaling pathways that are regulated by different concentrations of PACAP.

KW - ADNP

KW - Mouse

KW - Neuron/glia co-culture

KW - PACAP

KW - Signal transduction

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U2 - 10.1016/j.peptides.2006.01.007

DO - 10.1016/j.peptides.2006.01.007

M3 - 学術論文

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AN - SCOPUS:33744978998

SN - 0196-9781

VL - 27

SP - 1859

EP - 1864

JO - Peptides

JF - Peptides

IS - 7

ER -

Signaling involved in pituitary adenylate cyclase-activating polypeptide-stimulated ADNP expression

Abstract

Keywords

ASJC Scopus subject areas

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