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Chronic beta-adrenergic receptor stimulation enhances the expression of G-Protein coupled receptor kinases, GRK2 and GRK5, in both the heart and peripheral lymphocytes

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タイトル: Chronic beta-adrenergic receptor stimulation enhances the expression of G-Protein coupled receptor kinases, GRK2 and GRK5, in both the heart and peripheral lymphocytes
著者: Oyama, Naotsugu 著作を一覧する
Urasawa, Kazushi 著作を一覧する
Kaneta, Satoshi 著作を一覧する
Sakai, Hidetsugu 著作を一覧する
Saito, Takahiko 著作を一覧する
Takagi, Chika 著作を一覧する
Yoshida, Ichiro 著作を一覧する
Kitabatake, Akira 著作を一覧する
Tsutsui, Hiroyuki 著作を一覧する
キーワード: Catecholamine
G protein-coupled receptor kinase
Receptor down-regulation
発行日: 2005年 8月
出版者: The Japanese Circulation Society
誌名: Circulation Journal
巻: 69
号: 8
開始ページ: 987
終了ページ: 990
出版社 DOI: 10.1253/circj.69.987
抄録: Background: Enhanced expression of G protein-coupled receptor kinase (GRK) has been reported in failing hearts and in the present study the stability of enhanced GRK mRNA expression, and the correlation between the expression level of GRK mRNA in peripheral lymphocytes and in the heart were both evaluated. Methods and Results: Isoproterenol was injected into rats for 2 weeks, and then GRK5 mRNA was assessed by quantitative reverse transcriptase-palymerase chain reaction. An enhanced expression of cardiac GRK5 mRNA was observed even after 4 weeks of recovery. The isoproterenol-induced increased expression of GRK2 and GRK5 mRNA was equally observed in the heart and lymphocytes, and there was a close correlation between the heart and lymphocytes in the level of expression of each GRK mRNA. Conclusions: The GRK mRNA level is maintained at a high level for a long period without continuous β-adrenergic receptor stimulation. The level in circulating lymphocytes could be used as a surrogate marker to estimate the level of cardiac GRK expression and, presumably, the β-adrenergic receptor function of cardiomyocytes. (Circ J 2005; 69: 987-990)
資料タイプ: article (author version)
URI: http://hdl.handle.net/2115/17016
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 筒井 裕之

 

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