Elastin-derived peptides and TGF-beta1 induce osteogenic responses in smooth muscle cells.

Elastin degradation associated with matrix metalloproteinase activity is a cell-mediated process, observed in almost all types of vascular calcification. In this study, we tested the hypothesis that elastin-derived peptides induce an osteogenic response in vascular smooth muscle cells (SMCs) in vitro. Using RT-PCR and specific protein assays, we demonstrated that rat aortic SMCs incubated with elastin peptides exhibited an increased expression of the 67 kDa elastin laminin receptor (ELR) and matrix metalloproteinase-2 and typical bone proteins, such as core binding factor alpha-1, osteocalcin, and alkaline phosphatase. The osteogenic gene expression in SMCs was further enhanced by the addition of TGF-beta1 along with the elastin peptides, in the absence of any other mineralizing agent. Conversely, lactose (an ELR antagonist) down-regulated expression of most investigated proteins. In conclusion, elastin-derived peptides and TGF-beta1 up-regulate the expression of typical bone proteins in cultured rat aortic SMCs, possibly via the ELR signaling.