Abstract
Angiotensin II activates three major mitogen-activated protein kinases (MAPK) in vascular smooth muscle cells. Although other angiotensin II-induced MAPKs activation require transactivation of a growth factor receptor, the detailed mechanism by which angiotensin II activates c-Jun NH(2)-terminal kinase (JNK) remains unclear. Here, an immunosuppressant, cyclosporin A but not FK506, selectively inhibited angiotensin II-induced JNK activation in vascular smooth muscle cells. However, cyclosporin A had no inhibitory effect on angiotensin II-induced protein synthesis. Thus, angiotensin II-induced JNK activation but not protein synthesis is mediated by a mechanism sensitive to cyclosporin A, which is independent from calcineurin in vascular smooth muscle cells.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Angiotensin II / metabolism
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Angiotensin II / pharmacology*
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Animals
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Anisomycin / pharmacology
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Aorta, Thoracic
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Cells, Cultured
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Cyclosporine / pharmacology*
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Enzyme Activation / drug effects
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Enzyme Inhibitors / pharmacology
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Immunosuppressive Agents / pharmacology*
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JNK Mitogen-Activated Protein Kinases
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Leucine / metabolism
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Mitogen-Activated Protein Kinases / antagonists & inhibitors*
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Mitogen-Activated Protein Kinases / metabolism
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / metabolism
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Phosphorylation
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Protein Biosynthesis*
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Protein Synthesis Inhibitors / pharmacology
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Rats
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Rats, Sprague-Dawley
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Sulfonamides / pharmacology
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Tacrolimus / pharmacology
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p38 Mitogen-Activated Protein Kinases
Substances
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Enzyme Inhibitors
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Immunosuppressive Agents
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Protein Synthesis Inhibitors
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Sulfonamides
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Angiotensin II
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W 7
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Anisomycin
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Cyclosporine
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases
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p38 Mitogen-Activated Protein Kinases
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Leucine
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Tacrolimus