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The Journal of Clinical Investigation logoLink to The Journal of Clinical Investigation
. 1997 Dec 1;100(11):2824–2832. doi: 10.1172/JCI119830

Inhibition of rat vascular smooth muscle proliferation in vitro and in vivo by bone morphogenetic protein-2.

T Nakaoka 1, K Gonda 1, T Ogita 1, Y Otawara-Hamamoto 1, F Okabe 1, Y Kira 1, K Harii 1, K Miyazono 1, Y Takuwa 1, T Fujita 1
PMCID: PMC508488  PMID: 9389748

Abstract

Vascular 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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Selected References

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