Activation of Extracellular Signal-Activated Kinase by Angiotensin II-Induced Gq-Independent Epidermal Growth Factor Receptor Transactivation
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- MIURA Shin-ichiro
- Department of Cardiology, Fukuoka University School of Medicine
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- ZHANG Jingli
- Department of Molecular Cardiology, Lerner Research Institute Cleveland Clinic Foundation
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- MATSUO Yoshino
- Department of Cardiology, Fukuoka University School of Medicine
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- SAKU Keijiro
- Department of Cardiology, Fukuoka University School of Medicine
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- S. KARNIK Sadashiva
- Department of Molecular Cardiology, Lerner Research Institute Cleveland Clinic Foundation
書誌事項
- タイトル別名
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- <B>Activation of Extracellular Signal-Activated Kinase by Angiotensin II-Induced Gq-Independent Epidermal Growth Factor Receptor Transactivation</B>
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抄録
Multiple signaling pathways link the angiotensin II (Ang II) type 1 (AT1) receptor to Gq-dependent inositol phosphate (IP) production and Gq-independent phospho-extracellular signal-activated kinase (p-ERK) 1/2 activation by Ang II in the regulation of cardiovascular vasoconstriction and cell growth, respectively. An Ang II analogue, [Sar1, Ile4, Ile8]Ang II, did not stimulate Gq-dependent IP production, but still activated Gq-independent p-ERK1/2 in human coronary artery smooth muscle cells as well as in a cell line that stably expressed AT1. This activation was mostly mediated by [Sar1, Ile4, Ile8]Ang II-induced Gq-independent epidermal growth factor receptor transactivation. We found that AT1 receptor signaling shows bifurcation into functionally separate pathways. A clear understanding of this unique signaling may be necessary for the development of therapeutic agents to treat disorders such as hypertension and cardiac hypertrophy. (Hypertens Res 2004; 27: 765-770)
収録刊行物
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- Hypertension Research
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Hypertension Research 27 (10), 765-770, 2004
日本高血圧学会