Troglitazone inhibits angiotensin II-induced DNA synthesis and migration in vascular smooth muscle cells

FEBS Lett. 1997 Jan 2;400(1):119-21. doi: 10.1016/s0014-5793(96)01371-3.

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

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Angiotensin II / antagonists & inhibitors*
  • Angiotensin II / pharmacology
  • Animals
  • Aorta, Thoracic
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Cell Movement
  • Cells, Cultured
  • Chromans / pharmacology*
  • DNA / biosynthesis*
  • DNA / drug effects
  • Enzyme Activation
  • Hypoglycemic Agents / pharmacology*
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects*
  • Muscle, Smooth, Vascular / metabolism
  • Rats
  • Thiazoles / pharmacology*
  • Thiazolidinediones*
  • Troglitazone
  • Vasoconstrictor Agents / antagonists & inhibitors*
  • Vasoconstrictor Agents / pharmacology

Substances

  • Chromans
  • Hypoglycemic Agents
  • Thiazoles
  • Thiazolidinediones
  • Vasoconstrictor Agents
  • Angiotensin II
  • DNA
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Troglitazone