Heterotrimeric G Protein Gα_<13>-Induced Induction of Cytokine mRNAs Through Two Distinct Pathways in Cardiac Fibroblasts

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著者

    • FUKUTOMI Masashi
    • Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University
    • MARUYAMA Yoshiko
    • Laboratory of Cellular Signaling, Graduate School of Pharmaceutical Sciences, University of Tokyo
    • KOBAYASHI Hiroyuki
    • Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University
    • KUROSE Hitoshi
    • Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University

抄録

Overexpression of constitutively active (CA)-Gα<sub>13</sub> significantly increased the expression of interleukin (IL)-1β and IL-6 mRNAs and proteins in rat cardiac fibroblasts. IL-1β mRNA induction by CA-Gα<sub>13</sub> was suppressed by diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, but not by BAPTA-AM, an intracellular Ca<sup>2+</sup> chelator. In contrast, IL-6 mRNA induction by CA-Gα<sub>13</sub> was suppressed by BAPTA-AM but not by DPI. However, both IL-1β and IL-6 mRNA induction was suppressed by nuclear factor κB (NF-κB) inhibitors. The CA-Gα<sub>13</sub>-induced NF-κB activation was suppressed by DPI and BAPTA-AM, but not C3 toxin and the Rho-kinase inhibitor Y27632. IL-6 mRNA induction by CA-Gα<sub>13</sub> was suppressed by SK&F96365 (1-[β-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1<i>H</i>-imidazole hydrochloride), an inhibitor of receptor-activated nonselective cation channels, and the expression of CA-Gα<sub>13</sub> increased basal Ca<sup>2+</sup> influx. These results suggest that Gα<sub>13</sub> regulates IL-1β mRNA induction through the reactive oxygen species-NF-κB pathway, while it regulates IL-6 mRNA induction through the Ca<sup>2+</sup>-NF-κB pathway.<br>

収録刊行物

  • Journal of pharmacological sciences  

    Journal of pharmacological sciences 101(2), 144-150, 2006-06-20 

    The Japanese Pharmacological Society

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各種コード

  • NII論文ID(NAID)
    10018237777
  • NII書誌ID(NCID)
    AA11806667
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13478613
  • NDL 記事登録ID
    7963336
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  CJP引用  NDL  J-STAGE 
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