[HTML][HTML] Troglitazone inhibits angiotensin II-induced DNA synthesis and migration in vascular smooth muscle cells
K Graf, XP Xi, WA Hsueh, RE Law - FEBS letters, 1997 - Elsevier
K Graf, XP Xi, WA Hsueh, RE Law
FEBS letters, 1997•ElsevierAngiotensin 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 …
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 …
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.
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