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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  • Nigorikawa Kiyomi
    Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
  • Hazeki Kaoru
    Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
  • Kumazawa Takashi
    Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
  • Itoh Yuhta
    Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
  • Hoshi Megumi
    Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
  • Hazeki Osamu
    Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan

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Other Title
  • Class-ⅠA Phosphoinositide 3-Kinase p110β Triggers GPCR-Induced Superoxide Production in p110γ-Deficient Murine Neutrophils
  • Class-IA Phosphoinositide 3-Kinase p110^|^beta; Triggers GPCR-Induced Superoxide Production in p110^|^gamma;-Deficient Murine Neutrophils

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Abstract

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, p110γ. In the present study, we observed that the cells from p110γ−/− mice gain a response to N-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 (p110α, p110β, and p110δ) of PI3K are sufficient to trigger and maintain superoxide production. Examination of the effects of isoform-specific inhibitors suggested that the p110β isoform is the primary PI3K triggering the response to GPCR agonists when p110γ is absent.

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