ID 110683
Author
Miki, Mari Department of Internal Medicine and Molecular Therapeutics, The University of Tokushima School of Medicine|Department of Clinical Research, Kochi National Hospital
Nakamura, Yoichi Department of Clinical Research, Kochi National Hospital
Takahashi, Akira Department of Nutrition, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Nakaya, Yutaka Department of Nutrition, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Eguchi, Hiroshi Teijin Institute for Biomedical Research
Masegi, Tsukio Teijin Institute for Biomedical Research
Yoneda, Kazuo Department of Internal Medicine and Molecular Therapeutics, The University of Tokushima School of Medicine
Yasuoka, Susumu Department of Nutrition, The University of Tokushima School of Medicine
Sone, Saburo Department of Internal Medicine and Molecular Therapeutics, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
human airway trypsin-like protease (HAT)
human bronchial epithelial cells (HBEC)
protease-activated receptor-2(PAR-2)
intracellular calcium
Content Type
Journal Article
Description
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.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
50
Issue
1-2
Start Page
95
End Page
107
Sort Key
95
Published Date
2003
EDB ID
FullText File
language
eng
TextVersion
Publisher
departments
Medical Sciences