Role of protein kinase C-.DELTA. in isoproterenol-induced amylase release in rat parotid acinar cells

DOI Web Site 参考文献19件
  • Sugiya Hiroshi
    Department of Physiology, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo
  • Satoh Keitaro
    Department of Physiology, Nihon University School of Dentistry at Matsudo
  • Matsuki-Fukushima Miwako
    Department of Physiology, Nihon University School of Dentistry at Matsudo
  • Qi Bing
    Department of Physiology, Nihon University School of Dentistry at Matsudo
  • Guo Ming-Yu
    Department of Physiology, Nihon University School of Dentistry at Matsudo
  • Fujita-Yoshigaki Junko
    Department of Physiology, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo

抄録

In parotid acinar cells, β-adrenergic receptor activation results in accumulation of intracellular cAMP. Subsequently, cAMP-dependent protein kinase (PKA) is activated and consequently amylase release is provoked. In this paper, we investigated involvement of protein kinase C-δ (PKCδ), a novel isoform of PKC, in amylase release induced by β-adrenergic receptor stimulation. Amylase release stimulated with the β-agonsit isoproterenol (IPR) was inhibited by rottlerin, an inhibitor of PKCδ. IPR activated PKCδ and the effect of IPR were inhibited by a PKA inhibitor, H89. Myristoylated alanine-rich C kinase substrate (MARCKS), a major cellular substrate for PKC, was detected in rat parotid acinar cells, and a MARCKS inhibitor, MARCKS-related peptide, inhibited the IPR-induced amylase release. IPR stimulated MARCKS phosphorylation, which was found to be inhibited by H89 and rottlerin. These observations suggest that PKCδ activation is a downstream pathway of PKA activation and is involved in amylase release via MARCKS phosphorylation in rat parotid acinar cells stimulated with β-adrenergic agonist. J. Med. Invest. 56 Suppl.: 368-370, December, 2009

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