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Am J Physiol Heart Circ Physiol 284: H635-H643, 2003. First published October 10, 2002; doi:10.1152/ajpheart.00986.2001
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Vol. 284, Issue 2, H635-H643, February 2003

ANG II increases TIMP-1 expression in rat aortic smooth muscle cells in vivo

Giovanna Castoldi1,*, Cira R. T. di Gioia2,*, Federico Pieruzzi1, Cristina D'Orlando1, Willy M. M. van de Greef3, Giuseppe Busca1, Giovanni Sperti3, and Andrea Stella1

1 Unitá Didattico Assistenziale Nefrocardiovascolare, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università degli Studi di Milano-Bicocca 20052, Monza and Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore, Instituto di Ricovero e Cura a Carattere Scienti, 20100 Milan; 2 Dipartimento di Medicina Sperimentale e Patologia, Istituto di Anatomia Patologica, Università La Sapienza, 00161 Rome; and 3 Istituto di Cardiologia, Università Cattolica, 00168 Rome, Italy

Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are involved in tissue remodeling processes. TIMP-1 is the main native inhibitor of MMPs and it contributes to the development of tissue fibrosis. It is known that ANG II plays a fundamental role in vascular remodeling. In this study, we investigated whether ANG II modulates TIMP-1 expression in rat aortic smooth muscle cells. In vitro, ANG II induces TIMP-1 mRNA expression in a dose-dependent manner. The maximal increase in TIMP-1 expression was present after 3 h of ANG II stimulation. The ANG II increase in TIMP-1 expression was mediated by the ANG type 1 receptors because it was blocked by losartan. The increase in TIMP-1 expression was present after the first ANG II treatment, whereas repeated treatments (3 and 5 times) did not modify TIMP-1 expression. In vivo, exogenous ANG II was administered to Sprague-Dawley rats (200 ng · kg-1 · min-1 sc) for 6 and 25 days. Control rats received physiological saline. After treatment, systolic blood pressure was significantly higher (P < 0.01), whereas plasma renin activity was suppressed (P < 0.01), in ANG II-treated rats. ANG II increased TIMP-1 expression in the aorta of ANG II-treated rats both at the mRNA (P < 0.05) and protein levels as evaluated by Western blotting (P < 0.05) and/or immunohistochemistry. Neither histological modifications at the vascular wall nor differences in collagen content in the tunica media were present in both the ANG II- and saline-treated groups. Our data demonstrate that ANG II increases TIMP-1 expression in rat aortic smooth muscle cells. In vivo, both short- and long-term chronic ANG II treatments increase TIMP-1 expression in the rat aorta. TIMP-1 induction by ANG II in aortic smooth muscle cells occurs in the absence of histological changes at the vascular wall.

collagen; experimental hypertension; vessels

* G. Castoldi and C. R. T. di Gioia contributed equally to this study.




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