Regulation by Protein Kinase C of Platelet-Activating Factor- and Thapsigargin-Induced Calcium Entry in Rabbit Neutrophils.

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概要

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• 12-<I>O</I>-Tetradecanoylphorbol-13-acetate (TPA) time-dependently inhibited the platelet-activating factor (PAF)-induced rise in cytosolic free calcium concentration ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) in rabbit neutrophils, whereas staurosporine significantly enhanced it. Inositol 1, 4, 5-trisphosphate (IP<SUB>3</SUB>) induced Ca<SUP>2+</SUP> release in digitonin-permeabilized cells but not in PAF-pretreated permeabilized cells. IP<SUB>3</SUB>-induced Ca<SUP>2+</SUP> release was not affected by protein kinase C activators or inhibitors. In the cells pretreated with PAF and thapsigargin in Ca<SUP>2+</SUP>-deficient medium, stimulated Ca<SUP>2+</SUP> entry was evoked by the subsequent addition of CaCl<SUB>2</SUB>. TPA inhibited the Ca<SUP>2+</SUP> entry induced by PAF and thapsigargin in a staurosporine-reversible manner but not thapsigargin-induced [Ca<SUP>2+</SUP>]<SUB>i</SUB> elevation. These results suggest that protein kinase C negatively regulates PAF- and thapsigargin-induced rise in [Ca<SUP>2+</SUP>]<SUB>i</SUB> possibly by inhibiting Ca<SUP>2+</SUP> store depletion-induced Ca<SUP>2+</SUP> entry.

• 公益社団法人 日本薬理学会の論文

著者

• Morita Katsuya

  Department Of Dental Pharmacology Hiroshima University Graduate School Of Biomedical Sciences

• Kitayama Shigeo

  Department Of Dental Pharmacology

• Shibata Kazuyuki

  Department Of Biology School Of Education Waseda University

• Okamoto Hiroshi

  Department Of Advanced Biological Sciences For Regeneration (kotobiken Medical Laboratories) Tohoku

• MORITA Katsuya

  Department of Pharmacology, Hiroshima University School of Dentistry

• Dohi Toshihiro

  Department of Dental Pharmacology, Division of Integrated Medical Science, Hiroshima University Graduate School of Biomedical Sciences, Japan

• Shirakawa Masaharu

  Department of Endodontology and Periodontology, Hiroshima University School of Dentistry

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