Inhibition of superoxide anion production by extracellular acidification in neutrophils

Naoya Murata; Chihiro Mogi; Masayuki Tobo; Takashi Nakakura; Koichi Sato; Hideaki Tomura; Fumikazu Okajima

doi:10.1016/j.cellimm.2009.05.008

Inhibition of superoxide anion production by extracellular acidification in neutrophils

Naoya Murata, Chihiro Mogi, Masayuki Tobo, Takashi Nakakura, Koichi Sato, Hideaki Tomura, Fumikazu Okajima

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

39 Scopus citations

Abstract

Extracellular acidification inhibited formyl-Met-Leu-Phe- or C5a-induced superoxide anion (O₂^-) production in differentiated HL-60 neutrophil-like cells and human neutrophils. A cAMP-increasing agonist, prostaglandin E₁, also inhibited the formyl peptide-induced O₂^- production. The inhibitory action on the O₂^- production by extracellular acidic pH was associated with cAMP accumulation and partly attenuated by H89, a protein kinase A inhibitor. A significant amount of mRNAs for T-cell death-associated gene 8 (TDAG8) and other proton-sensing ovarian cancer G-protein-coupled receptor 1 (OGR1)-family receptors is expressed in these cells. These results suggest that cAMP/protein kinase A, possibly through proton-sensing G-protein-coupled receptors, may be involved in extracellular acidic pH-induced inhibition of O₂^- production.

Original language	English
Pages (from-to)	21-26
Number of pages	6
Journal	Cellular Immunology
Volume	259
Issue number	1
DOIs	https://doi.org/10.1016/j.cellimm.2009.05.008
State	Published - 2009
Externally published	Yes

Keywords

Acidification
cAMP
Neutrophil(s)
Proton-sensing
Superoxide anion
TDAG8

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.cellimm.2009.05.008

Cite this

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title = "Inhibition of superoxide anion production by extracellular acidification in neutrophils",

abstract = "Extracellular acidification inhibited formyl-Met-Leu-Phe- or C5a-induced superoxide anion (O2-) production in differentiated HL-60 neutrophil-like cells and human neutrophils. A cAMP-increasing agonist, prostaglandin E1, also inhibited the formyl peptide-induced O2- production. The inhibitory action on the O2- production by extracellular acidic pH was associated with cAMP accumulation and partly attenuated by H89, a protein kinase A inhibitor. A significant amount of mRNAs for T-cell death-associated gene 8 (TDAG8) and other proton-sensing ovarian cancer G-protein-coupled receptor 1 (OGR1)-family receptors is expressed in these cells. These results suggest that cAMP/protein kinase A, possibly through proton-sensing G-protein-coupled receptors, may be involved in extracellular acidic pH-induced inhibition of O2- production.",

keywords = "Acidification, cAMP, Neutrophil(s), Proton-sensing, Superoxide anion, TDAG8",

author = "Naoya Murata and Chihiro Mogi and Masayuki Tobo and Takashi Nakakura and Koichi Sato and Hideaki Tomura and Fumikazu Okajima",

year = "2009",

doi = "10.1016/j.cellimm.2009.05.008",

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volume = "259",

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journal = "Cellular Immunology",

issn = "0008-8749",

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number = "1",

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TY - JOUR

T1 - Inhibition of superoxide anion production by extracellular acidification in neutrophils

AU - Murata, Naoya

AU - Mogi, Chihiro

AU - Tobo, Masayuki

AU - Nakakura, Takashi

AU - Sato, Koichi

AU - Tomura, Hideaki

AU - Okajima, Fumikazu

PY - 2009

Y1 - 2009

N2 - Extracellular acidification inhibited formyl-Met-Leu-Phe- or C5a-induced superoxide anion (O2-) production in differentiated HL-60 neutrophil-like cells and human neutrophils. A cAMP-increasing agonist, prostaglandin E1, also inhibited the formyl peptide-induced O2- production. The inhibitory action on the O2- production by extracellular acidic pH was associated with cAMP accumulation and partly attenuated by H89, a protein kinase A inhibitor. A significant amount of mRNAs for T-cell death-associated gene 8 (TDAG8) and other proton-sensing ovarian cancer G-protein-coupled receptor 1 (OGR1)-family receptors is expressed in these cells. These results suggest that cAMP/protein kinase A, possibly through proton-sensing G-protein-coupled receptors, may be involved in extracellular acidic pH-induced inhibition of O2- production.

AB - Extracellular acidification inhibited formyl-Met-Leu-Phe- or C5a-induced superoxide anion (O2-) production in differentiated HL-60 neutrophil-like cells and human neutrophils. A cAMP-increasing agonist, prostaglandin E1, also inhibited the formyl peptide-induced O2- production. The inhibitory action on the O2- production by extracellular acidic pH was associated with cAMP accumulation and partly attenuated by H89, a protein kinase A inhibitor. A significant amount of mRNAs for T-cell death-associated gene 8 (TDAG8) and other proton-sensing ovarian cancer G-protein-coupled receptor 1 (OGR1)-family receptors is expressed in these cells. These results suggest that cAMP/protein kinase A, possibly through proton-sensing G-protein-coupled receptors, may be involved in extracellular acidic pH-induced inhibition of O2- production.

KW - Acidification

KW - cAMP

KW - Neutrophil(s)

KW - Proton-sensing

KW - Superoxide anion

KW - TDAG8

UR - https://www.scopus.com/pages/publications/68549117015

U2 - 10.1016/j.cellimm.2009.05.008

DO - 10.1016/j.cellimm.2009.05.008

M3 - 記事

C2 - 19539899

AN - SCOPUS:68549117015

SN - 0008-8749

VL - 259

SP - 21

EP - 26

JO - Cellular Immunology

JF - Cellular Immunology

IS - 1

ER -

Inhibition of superoxide anion production by extracellular acidification in neutrophils

Abstract

Keywords

UN SDGs

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