ID 110683
著者
ミキ, マリ Department of Internal Medicine and Molecular Therapeutics, The University of Tokushima School of Medicine|Department of Clinical Research, Kochi National Hospital
ナカムラ, ヨウイチ Department of Clinical Research, Kochi National Hospital
髙橋, 章 Department of Nutrition, The University of Tokushima School of Medicine 徳島大学 教育研究者総覧 KAKEN研究者をさがす
中屋, 豊 Department of Nutrition, The University of Tokushima School of Medicine 徳島大学 教育研究者総覧 KAKEN研究者をさがす
エグチ, ヒロシ Teijin Institute for Biomedical Research
マセギ, ツキオ Teijin Institute for Biomedical Research
ヨネダ, カズオ Department of Internal Medicine and Molecular Therapeutics, The University of Tokushima School of Medicine
安岡, 劭 Department of Nutrition, The University of Tokushima School of Medicine
曽根, 三郎 Department of Internal Medicine and Molecular Therapeutics, The University of Tokushima School of Medicine 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
human airway trypsin-like protease (HAT)
human bronchial epithelial cells (HBEC)
protease-activated receptor-2(PAR-2)
intracellular calcium
資料タイプ
学術雑誌論文
抄録
It has been shown that human airway trypsin-like protease (HAT) is localized in human bronchial epithelial cells (HBEC), and trypsin activates protease-activated receptor-2(PAR-2). Activation of PAR-2 activates G-protein followed by an increase of intracellular free Ca2+, [Ca2+]in. This study was undertaken to clarify whether HAT can activate PAR-2in HBEC or not. RT-PCR showed that HAT mRNA is expressed in HBEC, and PAR-2 mRNA is the most strongly expressed of the known PARs in HBEC. Both PAR-2 agonist peptide (PAR-2 AP) and HAT increased [Ca2+]in in HBEC in a biphasic fashion a prompt, sharp increase (peak I) and a sustained low plateau (peak II). PAR-2 AP over 100-200 μM and HAT over 200-300 mU/ml (0.08-0.12 μM) induced both peak I and II, and PAR-2 AP below100 μM and HAT below 200 mU/ml induced only peak II. Both PAR-2 AP-induced and HAT-induced peak I were induced by Ca2+ mobilization from intracellular stores, because they appeared even in Ca2+-free medium. Both PAR-2 AP-induced and HAT-induced peak II were induced by an influx of extracellular Ca2+, because they were abolished in Ca2+-free medium. The Ca2+ response to HAT was desensitized by exposure of HBEC to PAR-2 AP. These results indicate that HBEC have a functional PAR-2, and HAT regulates cellular functions of HBEC via activation of PAR-2.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
50
1-2
開始ページ
95
終了ページ
107
並び順
95
発行日
2003
EDB ID
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系