Abstract
Angiotensin II (AII) plays a crucial role in controlling the proliferation and migration of vascular smooth muscle cells (VSMCs). The present study was undertaken to determine if troglitazone (Tro) has an effect on the G-protein coupled signaling through AII type I (AT-1) receptors in cultured rat aortic VSMCs. AII-induced MAP kinase activation was inhibited 67.9% by Tro. AII-induced DNA synthesis and migration was completely inhibited by Tro or by the AT-1 receptor blocker irbesartan. The present study demonstrates that troglitazone inhibits AII-induced DNA synthesis, migration and MAP kinase activation in VSMCs which are important molecular events for the development of neointimal hyperplasia and atherosclerosis.
Publication types
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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 / antagonists & inhibitors*
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Angiotensin II / pharmacology
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Animals
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Aorta, Thoracic
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Cell Movement
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Cells, Cultured
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Chromans / pharmacology*
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DNA / biosynthesis*
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DNA / drug effects
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Enzyme Activation
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Hypoglycemic Agents / pharmacology*
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Muscle, Smooth, Vascular / cytology
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / metabolism
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Rats
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Thiazoles / pharmacology*
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Thiazolidinediones*
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Troglitazone
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Vasoconstrictor Agents / antagonists & inhibitors*
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Vasoconstrictor Agents / pharmacology
Substances
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Chromans
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Hypoglycemic Agents
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Thiazoles
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Thiazolidinediones
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Vasoconstrictor Agents
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Angiotensin II
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DNA
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Calcium-Calmodulin-Dependent Protein Kinases
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Troglitazone