Class-IA Phosphoinositide 3-Kinase p110<I>β</I> Triggers GPCR-Induced Superoxide Production in p110<I>γ</I>-Deficient Murine Neutrophils
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概要
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Studies with knockout mice have indicated that the only isoform of phosphoinositide 3-kinase (PI3K) functioning in the oxidative burst of mouse neutrophils in response to heterotrimeric guanine nucleotide-binding protein–coupled receptor (GPCR) agonists is a class-IB PI3K, p110<I>γ</I>. In the present study, we observed that the cells from p110<I>γ</I><SUP>－/－</SUP> mice gain a response to <I>N</I>-formyl-Met-Leu-Phe (fMLP) after priming with cytochalasin E. Even the unprimed cells, which show no response to fMLP, produce a significant amount of superoxide, when an effective agonist of the mouse-type fMLP receptors, Trp-Lys-Tyr-Met-Val-D-Met, is used to stimulate the cells. These results suggested that the class-IA isoforms (p110<I>α</I>, p110<I>β</I>, and p110<I>δ</I>) of PI3K are sufficient to trigger and maintain superoxide production. Examination of the effects of isoform-specific inhibitors suggested that the p110<I>β</I> isoform is the primary PI3K triggering the response to GPCR agonists when p110<I>γ</I> is absent.
- 公益社団法人 日本薬理学会の論文
著者
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Hazeki Osamu
Department Of Physiological Chemistry Graduate School Of Pharmaceutical Sciences The University Of T
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Hoshi Megumi
Department Of Pediatrics Dokkyo University School Of Medicine
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Kumazawa Takashi
Department Of Applied Chemistry Faculty Of Engineering Saitama Institute Of Technology
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Kumazawa Takashi
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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Itoh Yuhta
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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Hazeki Kaoru
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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Nigorikawa Kiyomi
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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Hazeki Osamu
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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Nigorikawa Kiyomi
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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ITOH Yuhta
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University
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HAZEKI Kaoru
Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University
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- Class-IA Phosphoinositide 3-Kinase p110β Triggers GPCR-Induced Superoxide Production in p110γ-Deficient Murine Neutrophils
- Class-IA Phosphoinositide 3-Kinase p110β Triggers GPCR-Induced Superoxide Production in p110γ-Deficient Murine Neutrophils