ID 111477
著者
Sugiya, Hiroshi Nihon University
Satoh, Keitaro Nihon University
Matsuki-Fukushima, Miwako Nihon University
Qi, Bing Nihon University
Guo, Ming-Yu Nihon University
Fujita-Yoshigaki, Junko Nihon University
キーワード
PKCδ
amylase release
MARCKS
parotid acinar cells
資料タイプ
学術雑誌論文
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.
掲載誌名
The Journal of Medical Investigation
ISSN
13496867
13431420
cat書誌ID
AA11166929
AA12022913
出版者
Faculty of Medicine Tokushima University
56
Supplement
開始ページ
368
終了ページ
370
並び順
368
発行日
2009-12
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版