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1 Division of Endocrinology, Department of Internal Medicine, University of California, Davis, CA, USA; Department of Veterans Affairs, Northern California Health Care System, Mather, CA, USA
2 Division of Endocrinology, Department of Internal Medicine, University of California, Davis, CA, USA
3 Division of Nephrology, Department of Internal Medicine, University of California, Davis, CA, USA; Department of Veterans Affairs, Northern California Health Care System, Mather, CA, USA; Cell and Developmental Biology Graduate Group, University of California, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: gawong{at}ucdavis.edu.
Bone morphogenetic proteins 2 and 7, multifunctional members of the TGF
superfamily with powerful osteoinductive effects, cause cell cycle arrest in a variety of transformed cell lines by activating signaling cascades that involve several cyclin dependent kinase inhibitors (CDKIs). CDKIs in the cip/kip family, p21Waf1/Cip1 and p27Kip1, have been shown to negatively regulate the G1 cyclins and their partner cyclin dependent kinase proteins resulting in BMP-mediated growth arrest. Bone morphogens have also been associated with antiproliferative effects in vascular tissue by unknown mechanisms. We now show that BMP2-mediated inhibition of PDGF-stimulated human aortic smooth muscle cell (HASMC) proliferation is accompanied by increased levels of p21 protein. Antisense oligodeoxynucleotides specific for p21
attenuated BMP2-induced inhibition of proliferation when transfected into HASMCs, demonstrating that BMP2 inhibits PDGF-stimulated proliferation of HASMCs, at least in part, through induction of p21. Whether p21-mediated induction of cell cycle arrest by BMP2 sets the stage for osteogenic differentiation of vascular smooth muscle cells,
ultimately leading to vascular mineralization, remains to be investigated.
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