ラット大動脈におけるMAPK依存性・ミオシンリン酸化非依存性のエンドセリン収縮
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概要
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エンドセリンは血管内皮細胞から産生される強力な血管収縮性ペプチドである。エンドセリンは高血はなどの循環器疾患に関与することが報告されているにもかかわらず,その血管収縮機構については未だに明らかでない点がある。一方,p42/43 MAPKとp38 MAPKは複数の成長ホルモンやストレスに応答して活性化されることが知られているが,エンドセリン-1による血管収縮機構における両MAPKの役割に関しては良くわかっていない。本研究では,p42/43MAPKとp38MAPKがエンドセリンー1による血管収縮機構に関与するか否かを検討した。ラット大動脈標本を作製し,CAF1OOにて等尺性収縮反応と細胞内Ca濃度を同時測定した。ミオシン軽鎖とp42/43 MAPK,およびp38MAPKのリン酸化をウエスタンプロットにて検出した。ラット大動脈において, ET-は持続性の収縮を生じたが,細胞内CaはET-lよって増加した後,時間経過に従って減少した。P42/43 MAPK阻害剤であるPD98059とp38MAKP阻害剤であるSB203580はいずれもET-l収縮を一部抑制した。ET-l刺激はp42/43MAPKとp38 MAPKのリン酸化を生じ,PD98059とSB203580はET-l刺激によるこれらのリン酸化を完全に抑制した。一方,PD98059とSB203580はET-によるミオシン軽鎖のリン酸化には全く影響しなかった。これらの成績からp42/43 MAPKのみならずp38 MAPKの両MAPK系がエンドセリンー1収縮をミオシンのリン酸化非依存性に一部制御していることが示唆された。
- 2003-02-25
著者
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Lee Won
Department of Internal Medicine, institute of Medical Research, Sungkyunkwan University School of Me
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Kim Bokyung
Department Of Physiology & Immunology School Of Medicine Konkuk University
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Kim B.
韓国
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Kim Bokyung
College Of Medicine Konkuk University
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KWON Seongchun
Department of Physiology, College of Medicine, Kwandong University
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FANG Lian
Department of Pharmacology, College of Medicine, Chungbuk University
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AHN Hee
Department of Pharmacology, College of Medicine, Chungbuk University
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Ahn Hee
Department Of Pharmacology College Of Medicine Chungbuk University
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Fang Lian
Department Of Pharmacology College Of Medicine Chungbuk University
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Kwon S
Department Of Physiology College Of Medicine Kwandong University
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Kwon Seongchun
Department Of Physiology College Of Medicine Yonsei University
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Lee Won
Department Of Agricultural And Biological Engineering University Of Florida
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Kim Bokyung
韓国
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Lee W
Department Of Pharmacology College Of Medicine Medical Research Institute Research Center For Biorcs
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KWON Scongchun
Department of Physiology,Kwandong University College of Medicine
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Ahn Hee
Department Of Chemistry And Center For Electro- And Photo-responsive Molecules Korea University
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KIM Bokyung
Department of Medicine, Konkuk University
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