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Am J Physiol Cell Physiol 282: C654-C664, 2002. First published November 27, 2001; doi:10.1152/ajpcell.00318.2001
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Vol. 282, Issue 4, C654-C664, April 2002

Angiotensin II AT2 receptor inhibits smooth muscle cell migration via fibronectin cell production and binding

Catherine Chassagne1,*, Christophe Adamy1,*, Philippe Ratajczak1, Bruno Gingras2, Emmanuel Teiger3, Emmanuelle Planus3, Patricia Oliviero1, Lydie Rappaport1, Jane-Lise Samuel1, and Sylvain Meloche2

1 Institut National de la Santé et de la Recherche Médicale (INSERM) U127, Institut Fédératif de Recherche Circulation Paris VII, Hôpital Lariboisière, Université Denis Diderot, 75475 Paris Cedex 10, France; 2 Institut de Recherches Cliniques de Montréal, Montreal, Quebec, H2W 1T8 Canada; and 3 INSERM U492, Institut de Médecine Moléculaire, Hôpital Henri-Mondor, 94010 Créteil Cedex, France

To explore the vascular function of the angiotensin II (ANG II) AT2 receptor subtype (AT2R), we generated a vascular smooth muscle cell (SMC) line expressing the AT2R (SMC-vAT2). The involvement of AT2R in the motility response of SMCs was examined in SMC-vAT2 cells and their controls (SMC-v) cultured on either laminin or fibronectin matrix proteins with the agarose drop technique. All experiments were conducted in the presence of a saturating concentration of losartan to inactivate the AT1R subtype. Under basal conditions, both cell lines migrated outside drops, but on laminin only. Treatment with ANG II significantly inhibited the migration of SMC-vAT2 but not SMC-v cells, and this effect was prevented by the AT2R antagonist CGP-42112A. The decreased migration of SMC-vAT2 was not associated with changes in cell growth, cytoskeleton stiffness, or smooth muscle actin, desmin, and tenascin expression. However, it was correlated with increased synthesis and binding of fibronectin. Both responses were prevented by incubation with selective AT2R antagonists. Addition of GRGDTP peptide, which prevents cell attachment of fibronectin, reversed the AT2R inhibitory effect on SMC-vAT2 migration. These results suggest that activated ANG II AT2R inhibits SMC migration via cellular fibronectin synthesis and associated cell binding.

vascular smooth muscle cells; laminin and fibronectin substrates; cellular fibronectin

* C. Chassagne and C. Adamy contributed equally to this work.




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