T Nakaoka, K Gonda, T Ogita, Y Otawara-Hamamoto, F Okabe, Y Kira, K Harii, K Miyazono, Y Takuwa, T Fujita
J Clin Invest.
1997;
100(11):2824–2832
doi:10.1172/JCI119830
This article Copyright © 1997, The American Society for Clinical Investigation
Abstract
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V
ascular proliferative disorders are characterized by the proliferation of vascular smooth muscle cells (SMCs) and excessive extracellular matrix synthesis. We found that bone morphogenetic protein-2 (BMP-2) inhibited serum-stimulated increases in DNA synthesis and cell number of cultured rat arterial SMCs in a fashion quite different from that in the case of transforming growth factor-beta1 (TGF-beta1). In addition, TGF-beta1 stimulated collagen synthesis in SMCs, whereas BMP-2 did not. In an in vivo rat carotid artery balloon injury model, the adenovirus-mediated transfer of the BMP-2 gene inhibited injury-induced intimal hyperplasia. These results indicate that BMP-2 has the ability to inhibit SMC proliferation without stimulating extracellular matrix synthesis, and suggest the possibility of therapeutic application of BMP-2 for the prevention of vascular proliferative disorders.
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