Molecular Mechanisms for α_2-Adrenoceptor-Mediated Regulation of Synoviocyte Populations
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概要
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The sympathetic nervous system has been indicated to influence the severity of inflammatory disease including rheumatoid arthritis. In this study, we elucidated the effects of catecholamine on the synovial cell populations. Stimulation with epinephrine or norepinephrine for 1 - 2 weeks dose- and time-dependently increased the number of synovial A (macrophage-like) cells but decreased that of B (fibroblast-like) cells. These responses in A and B cells were inhibited by the α2-antagonist yohimbine, the G-protein inactivator pertussis toxin and the phospholipase C (PLC) inhibitor U-73122. Furthermore, the protein kinase C (PKC) inhibitor calphostin C and mitogen-activated protein (MAP) kinase inhibitors PD98059 and wortmannin also abolished the norepinephrine effects on A and B cell numbers. In A cells cloned from an A and B cell mixture, norepinephrine also increased the cell number. In immunoblotting and immunocytostaining analyses, among the PKC isozymes, only PKC βII immunoreactivity was observed in the cytoplasm of unstimulated A and B cells. After α2-adrenoceptor stimulation, PKC βII immunoreactivity increased in the plasma membranes of both A and B cells with decreases in the cytoplasm. These findings indicated that α2-adrenoceptor stimulation of type A and B synoviocytes produced an increase and a decrease in the respective cell number, probably through Gi-coupled PLC activation and the resulting stimulation of the PKC βII/MAP kinase.
- 社団法人 日本薬理学会の論文
- 2001-03-01
著者
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Otani Hitomi
Department of Pharmacology, Kansai Medical University, Japan
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Inagaki Chiyoko
Department of Pharmacology, Kansai Medical University, Japan
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Otani Hitomi
Department Of Pharmacology Kansai Medical University
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Saito Naoaki
Laboratory of Molecular Pharmacology, Biosignal Research Center, Kobe University, Japan
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KAWASAKI Hiroshi
Department of Chemistry, Faculty of Science and Engineering, Saga University
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Inagaki C
Kansai Medical Univ. Osaka Jpn
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Inagaki Chiyoko
Department Of Biology Kyoto College Of Pharmacy
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Saito Naoaki
Laboratory Of Molecular Pharmacology Biosignal Research Center Kobe Univ.
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OGAWA Ryokei
Department of Orthopedics Kansai Medical University
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MISHIMA Katsuyuki
Department of Pharmacology, Kansai Medical University
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TANABE Takatoshi
Department of Orthopaedic Surgery, Kansai Medical University
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OSHIRO Akihiro
Department of Pharmacology, Kansai Medical University
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Ogawa R
Department Of Orthopaedic Surgery Kansai Medical University
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Ogawa Ryokei
Department Of Orthopaedic Surgery Kansai Medecal University
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Ogawa Ryokei
Department Of Orthopedic Surgery Kansai Medical University
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Oshiro Akihiro
Department Of Pharmacology Kansai Medical University
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Tanabe Takatoshi
Department Of Orthopaedic Surgery Kansai Medical University
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Mishima K
Department Of Pharmacology Kansai Medical University
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Kawasaki H
Department Of Pharmacology Kansai Medical University
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Kawasaki Hiroshi
Department Of Allergy And Rheumatology Research Hospital Institute Of Medical Science University Of
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Otani Hitomi
Dep. Of Pharmacology Kansai Medical Univ. Jpn
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INAGAKI Chiyoko
Departmctit of Pharmacology, Faculty of Medicine, Kyoto University
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